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Entity

Name
Wnt signaling pathway
Namespace
GOBP
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/go-biological-process/go-biological-process-20170725.belns

Appears in Networks 51

Anhedonia_Model_Deliverable_1.3 v0.1.3

Anhedonia Model with 110 new articles (including 5 full texts) from Klaus until 9th March

BEL Framework Large Corpus Document v20170611

Approximately 61,000 statements. This is a modified version of the original to use namespace files hosted on Artifactory

BEL Framework Small Corpus Document v20150611

Approximately 2000 hand curated statements drawn from 57 PubMeds.

TBI_SecondPart-QC v1.0.0

This knowledge assembly is specific to TBI for the TBI_cv_bio project

TBI_D1_CVBio_SCAI_13-04-2018 v2.3.28

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury (TBI). This version contains knowledge extracted from 306 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

TBI_D1_CVBio_SCAI_19-04-2018 v2.3.30

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury (TBI). This version contains knowledge extracted from 306 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

TBI_D1_CVBio_SCAI_22-04-2018 v2.3.31

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury (TBI). This version contains knowledge extracted from 306 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

TBI_D1_CVBio_SCAI_22-04-2018 v2.3.32

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury (TBI). This version contains knowledge extracted from 306 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

TBI_D1_CVBio_SCAI_25-04-2018 v2.3.33

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury (TBI). This version contains knowledge extracted from 306 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v1.0.0

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.1

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.8

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.9

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.10

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.11

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.12

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.15

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.16

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.17

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Anhedonia_Model_Deliverable_1.3 v0.2.4

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.5

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.6

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.0

Anhedonia Model Complete coding until 14th of May.

PTSD and TBI BEL Model v1.0.20

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Colorectal Cancer Knowledge Assembly - Drugs Pathways and General Biology v1.1.0

Colorectal Cancer Knowledge Assembly with drug associations and Pathways + general CRC biology

Anhedonia_Model_Final v1.0.1

Anhedonia Model Complete coding until 14th of May.

PTSD and TBI BEL Model v1.0.22

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.23

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.24

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Anhedonia_Model_Final v1.0.2

Anhedonia Model Complete coding generated from an equivalent of 421 articles (321 abstracts+10 full text (*10 abstracts)). It also contains part of projection models, since all the statements with non projection information discarded from projection model.

PTSD and TBI BEL Model v1.0.25

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

TBI BEL Model v1.0.27

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury. This version contains knowledge extracted from 523 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

TBRD - PTSD and TBI BEL Model v1.0.30

TBRD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI). This version contains knowledge extracted from 847 pubmed articles and 2 articles from other sources like Book. Out of these,523 articles belongs 323 PTSD articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Alzheimer's Disease Knowledge Assembly v5.0.6

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

Alzheimer's Disease Knowledge Assembly v5.0.9

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

colorectal cancer Knowledge Assembly - Drugs v1.0.1

colorectal cancer Knowledge Assembly with drug associations.

Colorectal Cancer Model v1.0.0

Colorectal Cancer Model built for i:DSem-BMBF project.

colorectal cancer Drugs resistance v1.0.1.0

colorectal cancer Knowledge Assembly with drug associations.

CRC_combined v1.1

BEL Document

Colorectal Cancer Model v2.0.0

Colorectal Cancer Model

Colorectal Cancer Model v0.0.0

Colorectal Cancer Model

Colorectal Cancer Model v2.0.3

Colorectal Cancer Model

Colorectal Cancer Model v2.0.4

Colorectal Cancer Model, uploaded by reagon

Colorectal Cancer Model v2.0.5

Colorectal Cancer Model, uploaded by reagon

Colorectal Cancer Model v2.0.6

Colorectal Cancer Model, uploaded by reagon

30232325 v2.0.4

test BEl doc.

30232325 v2.0.6

test BEl doc.

30232325.bel v2.0.2

test BEl doc.

30232325.bel v2.0.4

test BEl doc.

In-Edges 156

path(MESHF:"Stress, Psychological") regulates bp(GOBP:"Wnt signaling pathway")

In particular we found that stress and antidepressant treatment affected intracellular cascades like growth factor receptor signaling, G-protein-coupled receptor signaling, and Wnt signaling - processes involved in the neuroplastic changes observed during the progression of depression and antidepressant treatment. PubMed:24339877

a(CHEBI:antidepressant) regulates bp(GOBP:"Wnt signaling pathway")

In particular we found that stress and antidepressant treatment affected intracellular cascades like growth factor receptor signaling, G-protein-coupled receptor signaling, and Wnt signaling - processes involved in the neuroplastic changes observed during the progression of depression and antidepressant treatment. PubMed:24339877

bp(MESHPP:"Neuronal Plasticity") association bp(GOBP:"Wnt signaling pathway")

In particular we found that stress and antidepressant treatment affected intracellular cascades like growth factor receptor signaling, G-protein-coupled receptor signaling, and Wnt signaling - processes involved in the neuroplastic changes observed during the progression of depression and antidepressant treatment. PubMed:24339877

p(MGI:Foxl1) decreases bp(GOBP:"Wnt signaling pathway")

Foxl1 is a winged helix transcription factor expressed in the mesenchyme of the gastrointestinal tract. Foxl1 null mice display severe structural defects in the epithelia of the stomach, duodenum, and jejunum. Here we addressed the molecular mechanisms by which Foxl1 controls gastrointestinal differentiation. First we showed that the abnormalities found in the epithelia of the null mice are the result of an increase in the number of proliferating cells and not a change in the rate of cell migration. Next we investigated the regulatory circuits affected by Foxl1. We focused on the Wnt/beta-catenin signaling pathway as a possible target of Foxl1 as it has been shown to play a central role in gastrointestinal proliferation. We demonstrated that Foxl1 activates the Wnt/beta-catenin pathway by increasing extracellular proteoglycans, which act as co-receptors for Wnt. Thus we establish that Foxl1 is involved in the regulation of the Wnt/beta-catenin pathway, providing a novel link in mesenchymal/epithelial cross-talk in the gut. Moreover, we provide the first example implicating proteoglycans in the regulation of cellular proliferation in the gastrointestinal tract. PubMed:11555641

Annotations
Experimental Factor Ontology (EFO)
NCI-H460 cell
NCBI Taxonomy Ids
10090
Uberon
alimentary part of gastrointestinal system
Cell Ontology (CL)
macrophage
MeSH
Cytoplasm
Disease Ontology (DO)
medulloblastoma

p(MGI:Foxl1) decreases bp(GOBP:"Wnt signaling pathway")

Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. A previous study has demonstrated that Foxl1 is involved in the regulation of the beta-catenin signaling pathway (26). We also confirmed that the nuclear beta-catenin translocation was enhanced in the small intestinal epithelium of Foxl1–/– mice by Western blot analysis (Fig. 5). PubMed:16469829

Annotations
Experimental Factor Ontology (EFO)
U-937 cell
NCBI Taxonomy Ids
10090
Uberon
alimentary part of gastrointestinal system
Cell Ontology (CL)
hepatocyte
MeSH
Cell Membrane
Disease Ontology (DO)
squamous cell carcinoma
MeSH
Sputum
MeSH
Head and Neck Neoplasms

p(MGI:Crebbp) increases bp(GOBP:"Wnt signaling pathway")

Low-molecular-weight compounds that target transcriptional co-activators of the Wnt pathway such as BCL9, CBP, CREB, BRG1, Pygopus, Hyrax and components of the Mediator complex are also under scrutiny for potential therapeutic applications176,177 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
NCI-H69 cell
NCBI Taxonomy Ids
10090
Uberon
breast
Cell Ontology (CL)
stem cell
MeSH
Cell Nucleus
Disease Ontology (DO)
cancer
MeSH
Sputum
MeSH
Head and Neck Neoplasms

act(p(HGNC:SOX7), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

In view of these and other findings, we suggest different modes of action for SOX7 inside the cell including repression of Wnt signalling. PubMed:11691915

Annotations
Experimental Factor Ontology (EFO)
MCF7 cell
NCBI Taxonomy Ids
9606
Uberon
pancreas
Cell Ontology (CL)
leukocyte
MeSH
Cytoplasm
Disease Ontology (DO)
breast cancer

act(p(MGI:Hbp1), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

2.3. Gene targets We and several other laboratories have identified diverse target genes for HBP1. The nature of the genes provides major clues on how HBP1 might regulate signaling pathways in cancer. In each section, the significance of a given pathway to cancer or cell cycle progression will be highlighted. As described at the end of the review, HBP1 is a likely tumor suppressor gene with the recent identification of cancer-associated variants. Thus, consideration of HBP1 functions in signaling pathways that are associated with cancer has added significance. 2.3.1. Wnt target genes (Cyclin D1 and c-MYC) Our studies reveal that HBP1 is a general suppressor of Wnt signaling. PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
10090
Uberon
skeletal muscle tissue
Cell Ontology (CL)
dendritic cell
MeSH
Cell Nucleus
Disease Ontology (DO)
estrogen-receptor negative breast cancer

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Figure 6 Notch function in cervical cancer. A theoretical model of how the tumour-suppressor properties of NOTCH1 can, in principle, be sidestepped in HPV-infected cervical cancer cells, allowing manifestation of growth-promoting properties of NOTCH1. Apart from HPV E6 and E7 proteins, cervical cancers frequently express increased levels of the phosphatidylinositol 3-kinase (PI3K) subunit p110? and ?Np63 as a result of amplification of the q26-29 locus of chromosome 3. Experiments show that Notch-induced PI3K confers resistance to anoikis in epithelial cells. Whether ERBB2 is induced by NOTCH in cervical cancer remains to be elucidated. PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
Hep G2 cell
NCBI Taxonomy Ids
9606
Uberon
brown adipose tissue
Cell Ontology (CL)
cardiac muscle cell
MeSH
Cell Nucleus
Disease Ontology (DO)
lung cancer

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
Hep G2 cell
NCBI Taxonomy Ids
9606
Uberon
zone of skin
Cell Ontology (CL)
cardiac muscle cell
MeSH
Cell Nucleus
Disease Ontology (DO)
lung cancer

act(p(HGNC:CTNNB1), ma(tscript)) increases bp(GOBP:"Wnt signaling pathway")

Entrez Gene summary: Rat: SUMMARY: AXIN2 inhibits axis formation; acts as a negative regulator of the Wnt signaling pathway by inducing GSK-3beta-dependent phosphorylation of beta-catenin [RGD] Other:J Biol Chem 2004 Sep 24 279(39) 40255-8

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
skeletal muscle tissue
Cell Ontology (CL)
neuron
MeSH
Cell Nucleus
Disease Ontology (DO)
melanoma

act(p(HGNC:CTNNB1), ma(tscript)) increases bp(GOBP:"Wnt signaling pathway")

The Wnt/beta-catenin pathway rapidly induces the transcription of the cell-type-restricted transcription factor Pitx2 that is required for effective cell-specific proliferation activating growth-regulating genes PubMed:14636578

Annotations
Experimental Factor Ontology (EFO)
SW480 cell
NCBI Taxonomy Ids
9606
Uberon
aorta
Cell Ontology (CL)
Purkinje cell
MeSH
Cell Membrane
Disease Ontology (DO)
lung cancer

p(MGI:Notch1) decreases bp(GOBP:"Wnt signaling pathway")

NotchIC decreased Wnt/beta-catenin signaling. PubMed:12960086

Annotations
Experimental Factor Ontology (EFO)
3T3-L1 cell
NCBI Taxonomy Ids
10090
Uberon
adipose tissue
Cell Ontology (CL)
osteoblast
MeSH
Cytoplasm
Disease Ontology (DO)
leukemia

p(MGI:Notch1) decreases bp(GOBP:"Wnt signaling pathway")

Notch1 can also function as a tumour suppressor in mouse skin by inducing Waf1 and repressing Shh and Wnt signalling. PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
Hep G2 cell
NCBI Taxonomy Ids
10090
Uberon
zone of skin
Cell Ontology (CL)
cardiac muscle cell
MeSH
Cell Nucleus
Disease Ontology (DO)
lung cancer

p(MGI:Notch1) decreases bp(GOBP:"Wnt signaling pathway")

Notch1 function in mouse skin. Representation of mammalian skin with several layers of differentiating cells, and some proteins that are expressed in specific cellular layers. After differentiation signals are received, Notch1 induces expression of involucrin, keratin-1 (K1) and the cell-cycle inhibitor Waf1, and prevents the onset of fillagrin and loricrin expression until the cell is at later stages of differentiation. Both ?-catenin-mediated Wnt signalling and Gli2-mediated Sonic-hedgehog signalling are normally repressed in the murine epidermis by Notch1. In Notch1-ablated skin, re-activation of Wnt and Sonic-hedgehog pathways result in the development of basal-cell-carcinoma-like tumours in the mouse. PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
Hep G2 cell
NCBI Taxonomy Ids
10090
Uberon
zone of skin
Cell Ontology (CL)
cardiac muscle cell
MeSH
Cell Nucleus
Disease Ontology (DO)
lung cancer

act(p(MGI:Apc), ma(cat)) decreases bp(GOBP:"Wnt signaling pathway")

Moreover, PSD-95 can form a ternary complex with Frizzled-2 and the adenomatous polyposis coli protein, a negative regulator of Wnt signaling, suggesting that members of the PSD-95 family may serve to recruit intracellular signaling molecules of the Wnt/Frizzled pathway into the vicinity of the receptor. PubMed:12067714

Annotations
Experimental Factor Ontology (EFO)
Caco-2 cell
NCBI Taxonomy Ids
10090
Uberon
brain
Cell Ontology (CL)
smooth muscle cell
MeSH
Cell Nucleus
Disease Ontology (DO)
lymphoma

act(p(HGNC:RAC1), ma(gtp)) increases bp(GOBP:"Wnt signaling pathway")

Expression of dominant-negative (N17)Rac1 mutant in colon cancer cells caused a marked inhibition of Wnt signaling, as determined by the TCF/LEF-responsive (TOPFLASH) transcription assay. PubMed:15377999

Annotations
Experimental Factor Ontology (EFO)
SK-OV-3 cell
NCBI Taxonomy Ids
9606
Uberon
liver
Cell Ontology (CL)
fibroblast
MeSH
Extracellular Space
Disease Ontology (DO)
brain glioma
MeSH
Hypercholesterolemia

act(p(HGNC:HBP1), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Here, we show that HBP1 is a repressor of the cyclin D1 gene and inhibits the Wnt signaling pathway. PubMed:11500377

Annotations
Experimental Factor Ontology (EFO)
COS-1 cell
NCBI Taxonomy Ids
9606
Uberon
female gonad
Cell Ontology (CL)
thymocyte
MeSH
Cytoplasm
Disease Ontology (DO)
multiple myeloma

p(HGNC:TGFB1) decreases bp(GOBP:"Wnt signaling pathway")

TCF/LEF transcription factors with the HMG3 box are implicated in the WNT signaling pathway and are antagonized by the transforming growth factor beta signaling pathway PubMed:11085512

Annotations
Experimental Factor Ontology (EFO)
SK-OV-3 cell
NCBI Taxonomy Ids
9606
Uberon
endothelium
Cell Ontology (CL)
keratinocyte
MeSH
Cytoplasm
Disease Ontology (DO)
lung cancer

p(MGI:Kremen1) decreases bp(GOBP:"Wnt signaling pathway")

DKK1 antagonizes Wnt signalling during head formation in mice77. An additional DKK-receptor, Kremen, was shown to inhibit the Wnt signalling pathway by internalization of LRP PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
head
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Hematopoietic Stem Cells

path(MESHD:Neoplasms) positiveCorrelation bp(GOBP:"Wnt signaling pathway")

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
breast
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

path(MESHD:Neoplasms) positiveCorrelation bp(GOBP:"Wnt signaling pathway")

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

p(HGNC:RSPO1) increases bp(GOBP:"Wnt signaling pathway")

secreted proteins such as Norrin and R-Spondin were shown to be activators of the canonical Wnt pathway owing to their interaction with Frizzled–LRP receptors79,80 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
endothelium
Cell Ontology (CL)
keratinocyte
MeSH
Cell Membrane
Disease Ontology (DO)
atherosclerosis
MeSH
Urinary Bladder

p(HGNC:WNT2B) increases bp(GOBP:"Wnt signaling pathway")

In recent years, other mechanisms of activation of the canonical Wnt pathway in tumours have been discovered; for example, silencing of the genes that encode the inhibitory Wnt ligands SFRPs and DKKs by hypermethylation, or by overexpression of Wnt proteins (WNT2B for example), Frizzleds (FZD10 for example) or Dishevelled142-149 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
breast
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Urinary Bladder

p(HGNC:CCND1) positiveCorrelation bp(GOBP:"Wnt signaling pathway")

Increased Cyclin D1 levels in breast cancer cell lines and tumors have been correlated with increased β-catenin accumulation and constitutive Wnt signaling (Lin et al., 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

p(HGNC:FZD10) increases bp(GOBP:"Wnt signaling pathway")

In recent years, other mechanisms of activation of the canonical Wnt pathway in tumours have been discovered; for example, silencing of the genes that encode the inhibitory Wnt ligands SFRPs and DKKs by hypermethylation, or by overexpression of Wnt proteins (WNT2B for example), Frizzleds (FZD10 for example) or Dishevelled142-149 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
breast
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Urinary Bladder

p(MGI:Dkk1) decreases bp(GOBP:"Wnt signaling pathway")

DKK1 antagonizes Wnt signalling during head formation in mice77. An additional DKK-receptor, Kremen, was shown to inhibit the Wnt signalling pathway by internalization of LRP PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
head
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Hematopoietic Stem Cells

p(SFAM:"DVL Family") increases bp(GOBP:"Wnt signaling pathway")

In recent years, other mechanisms of activation of the canonical Wnt pathway in tumours have been discovered; for example, silencing of the genes that encode the inhibitory Wnt ligands SFRPs and DKKs by hypermethylation, or by overexpression of Wnt proteins (WNT2B for example), Frizzleds (FZD10 for example) or Dishevelled142-149 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
breast
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Urinary Bladder

p(HGNC:NDP) increases bp(GOBP:"Wnt signaling pathway")

secreted proteins such as Norrin and R-Spondin were shown to be activators of the canonical Wnt pathway owing to their interaction with Frizzled–LRP receptors79,80 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
endothelium
Cell Ontology (CL)
keratinocyte
MeSH
Cell Membrane
Disease Ontology (DO)
atherosclerosis
MeSH
Urinary Bladder

path(MESHD:"Stress Disorders, Traumatic") association bp(GOBP:"Wnt signaling pathway")

Differentially regulated transcripts in the AY, HC and MPFC across four time points were significantly associated with inflammatory pathways (TNF-α, IFN-γ, IL-6, chemokine, and TLR signaling and NF-κB transcriptional activities), as well as other important signaling pathways such as histone modifications, oxidative stress, neuronal growth factors, and WNT, NOTCH, β-catenin and cyclic AMP signaling pathways (Figure 3a). PubMed:28534873

path(MESHD:"Stress Disorders, Traumatic") association bp(GOBP:"Wnt signaling pathway")

Differentially regulated transcripts in the AY, HC and MPFC across four time points were significantly associated with inflammatory pathways (TNF-α, IFN-γ, IL-6, chemokine, and TLR signaling and NF-κB transcriptional activities), as well as other important signaling pathways such as histone modifications, oxidative stress, neuronal growth factors, and WNT, NOTCH, β-catenin and cyclic AMP signaling pathways (Figure 3a). PubMed:28534873

path(MESHF:"Stress Disorders, Post-Traumatic") increases bp(GOBP:"Wnt signaling pathway")

Interestingly, however, pathways related to CD3, CD4, CTLA4, TOB1, IDO1 and TGFB signaling were suppressed, suggesting inhibited T-helper cell-type-2 immunity (Figure 1b; Supplementary Table 3), whereas most immune responses were activated. Biological processes related to neurogenesis, synaptic plasticity, learning or memory, mTOR, NOTCH and calcium signaling were inhibited, whereas apoptosis of neurons, WNT- and cyclic AMP signaling was activated at later post-trauma periods (Figure 2a). PubMed:28534873

Annotations
NCBI Taxonomy Ids
10090
TBI_D1_CVBio_SCAI_8-3-2018
Result

path(MESHF:"Stress Disorders, Post-Traumatic") increases bp(GOBP:"Wnt signaling pathway")

Interestingly, however, pathways related to CD3, CD4, CTLA4, TOB1, IDO1 and TGFB signaling were suppressed, suggesting inhibited T-helper cell-type-2 immunity (Figure 1b; Supplementary Table 3), whereas most immune responses were activated. Biological processes related to neurogenesis, synaptic plasticity, learning or memory, mTOR, NOTCH and calcium signaling were inhibited, whereas apoptosis of neurons, WNT- and cyclic AMP signaling was activated at later post-trauma periods (Figure 2a). PubMed:28534873

g(HGNC:OVOL2) decreases bp(GOBP:"Wnt signaling pathway")

OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-β-catenin complex. Strategies to increase levels of OVOL2 might be developed to reduce colorectal tumor progression and metastasis. PubMed:26619963

g(HGNC:APC) association bp(GOBP:"Wnt signaling pathway")

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

path(MESHD:"Colorectal Neoplasms") negativeCorrelation bp(GOBP:"Wnt signaling pathway")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

p(HGNC:CHD4) decreases bp(GOBP:"Wnt signaling pathway")

We find that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of TSGs, suggesting that their combined inhibition may be beneficial for the treatment of colon cancer. PubMed:23708667

path(MESHD:Neoplasms) association bp(GOBP:"Wnt signaling pathway")

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

p(HGNC:WIF1) decreases bp(GOBP:"Wnt signaling pathway")

Several secreted protein families antagonize or modulate Wnt/beta-catenin signaling. sFRPs (secreted Frizzled related proteins), and WIF (Wnt inhibitory protein) bind to Wnt, and in the case of sFRPs, also to Fz,and thereby function as Wnt antagonists for both beta-catenin and non-canonical signaling PubMed:19619488

a(CHEBI:rosiglitazone) association bp(GOBP:"Wnt signaling pathway")

Rosiglitazone is a TZD derivative that was recently observed to improve cognition in both APP transgenic mice and AD patients [Watson et al., 2005; Pedersen et al., 2006]. It activates PPARgamma leading to increased glucose disposal rates [Jung et al., 2005] and is also neuroprotective against Abeta neurotoxicity [Inestrosa et al., 2005]. Neuroprotection may result through modulation of Wnt signaling since an increase in beta-catenin and inhibition of GSK-3beta is observed upon exposure to rosiglitazone [Inestrosa et al., 2005], although a different study has shown that activation of PPARgamma by a potent ligand leads to beta-catenin degradation [Liu and Farmer 2004]. Nonetheless, in support of the role for PPARgamma activation in neuroprotection, PPARgamma agonists have potent anti-inflammatory effects [Luna-Medina et al., 2005], inhibit microglial activation [Bernardo et al., 2005; Heneka et al., 2005] and have been shown to improve verbal memory in AD patients with T2DM, possibly in a mechanism dependent on PPARgamma activation . A recent report demonstrates that overexpression of PPARgamma in cultured cells leads to a dramatic decrease in the production of Abeta, by increasing the rate of APP degradation via ubiquitination [D'Abramo et al., 2005]. This study also showed that by decreasing Abeta secretion, PPARgamma protects the cells against H2O2-mediated necrosis [D'Abramo et al., 2005]. PubMed:19885299

bp(GOBP:"brain development") association bp(GOBP:"Wnt signaling pathway")

The Wnt signaling pathway plays a crucial role in the proper development and maintenance of brain and bone structure and function. PubMed:26880631

bp(GOBP:"brain development") association bp(GOBP:"Wnt signaling pathway")

Growing evidence indicates that wingless-type (Wnt) signaling plays an important role in neuronal development, synapse formation and synaptic plasticity. PubMed:26032671

bp(GOBP:neurogenesis) association bp(GOBP:"Wnt signaling pathway")

Several components in the Wnt signaling pathway, including beta-catenin and glycogen synthase kinase 3 beta, have been implied in AD pathogenesis. Here, mRNA brain levels from five-month-old tg-ArcSwe and nontransgenic mice were compared using Affymetrix microarray analysis. With surprisingly small overall changes, Wnt signaling was the most affected pathway with altered expression of nine genes in tg-ArcSwe mice. When analyzing mRNA levels of these genes in human brain, transcription factor 7-like 2 (TCF7L2) and v-myc myelocytomatosis viral oncogene homolog (MYC), were increased in Alzheimer's disease (AD) (P < .05). Furthermore, no clear differences in TCF7L2 and MYC mRNA were found in brains with frontotemporal lobar degeneration, suggesting that altered regulation of these Wnt-related genes could be specific to AD. Finally, mRNA levels of three neurogenesis markers were analyzed. Increased mRNA levels of dihydropyrimidinase-like 3 were observed in AD brain, suggesting that altered Wnt signaling pathway regulation may signify synaptic rearrangement or neurogenesis. PubMed:21234373

a(CHEBI:estrogen) increases bp(GOBP:"Wnt signaling pathway")

Along these lines, one mechanism through which E2 protects the hippocampus from cerebral ischemia is by preventing the post-ischemic elevation of Dkk1, a neurodegenerative factor that serves as an antagonist of the canonical Wnt signaling pathway, and simultaneously inducing pro-survival Wnt/beta-Catenin signaling in hippocampal neurons. PubMed:23261660

g(HGNC:CYLD) decreases bp(GOBP:"Wnt signaling pathway")

A positive role of K63-linked ubiquitylation was recently uncovered by the identification of the DUB enzyme and tumor suppressor CYLD as a negative regulator of upstream Wnt/beta-catenin signaling. PubMed:20930545

p(SFAM:"DVL Family") increases bp(GOBP:"Wnt signaling pathway")

Alzheimer's disease (AD) is a neurodegenerative disease with progressive dementia accompanied by three main structural changes in the brain: diffuse loss of neurons; intracellular protein deposits termed neurofibrillary tangles (NFT) and extracellular protein deposits termed amyloid or senile plaques, surrounded by dystrophic neurites. Recent studies have suggested that the trafficking process of membrane associated proteins is modulated by the FAD-linked presenilin (PS) proteins, and that amyloid beta-peptide deposition may be initiated intracellularly, through the secretory pathway. Current hypotheses concerning presenilin function are based upon its cellular localization and its putative interaction as macromolecular complexes with the cell-adhesion/signaling beta-catenin molecule and the glycogen synthase kinase 3beta (GSK-3beta) enzyme. Developmental studies have shown that PS proteins function as components in the Notch signal transduction cascade and that beta-catenin and GSK-3beta are transducers of the Wnt signaling pathway. Both pathways are thought to have an important role in brain development, and they have been connected through Dishevelled (Dvl) protein, a known transducer of the Wnt signaling pathway. In addition to a review of the current state of research on the subject, we present a cell signaling model in which a sustained loss of function of Wnt signaling components would trigger a series of misrecognition events, determining the onset and development of AD. PubMed:10967351

bp(GOBP:"regulation of bone development") association bp(GOBP:"Wnt signaling pathway")

The Wnt signaling pathway plays a crucial role in the proper development and maintenance of brain and bone structure and function. PubMed:26880631

p(HGNC:FRZB) decreases bp(GOBP:"Wnt signaling pathway")

Several secreted protein families antagonize or modulate Wnt/beta-catenin signaling. sFRPs (secreted Frizzled related proteins), and WIF (Wnt inhibitory protein) bind to Wnt, and in the case of sFRPs, also to Fz,and thereby function as Wnt antagonists for both beta-catenin and non-canonical signaling PubMed:19619488

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

Although the mechanism of Ab action in the pathogenesis of Alzheimer’s disease (AD) has remained elusive, it is known to increase the expression of the antagonist of canonical wnt signalling, Dickkopf-1 (Dkk1), whereas the silencing of Dkk1 blocks Ab neurotoxicity. PubMed:23164821

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

Caricasole et al demonstrated that the Abeta peptide fragment, Abeta25-35, induces neuronal expression of the wnt antagonist Dkk1 and that silencing of DKK1 blocks Abeta neurotoxicity. PubMed:23164821

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

We identify possible links with Dickkopf-1, a negative regulator of the wnt pathway, and propose that the abnormal expression of Keratin 9 in AD blood and cerebrospinal fluid may be a result of blood brain barrier dysregulation and disruption of the ubiquitin proteasome system. PubMed:26973255

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

More importantly, persistent activation of Wnt signaling through Wnt ligands, or inhibition of negative regulators of Wnt signaling, such as Dickkopf-1 (DKK-1) and glycogen synthase kinase-3 beta (GSK-3 beta ) that are hyperactive in the disease state, is able to protect against Abeta toxicity and ameliorate cognitive performance in AD. PubMed:24883305

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

Along these lines, one mechanism through which E2 protects the hippocampus from cerebral ischemia is by preventing the post-ischemic elevation of Dkk1, a neurodegenerative factor that serves as an antagonist of the canonical Wnt signaling pathway, and simultaneously inducing pro-survival Wnt/beta-Catenin signaling in hippocampal neurons. PubMed:23261660

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

Although the mechanism of Abeta action in the pathogenesis of Alzheimer's disease (AD) has remained elusive, it is known to increase the expression of the antagonist of canonical wnt signalling, Dickkopf-1 (Dkk1) PubMed:23164821

Annotations
NeuroMMSigDB
DKK1 subgraph

p(HGNC:CTNNB1) association bp(GOBP:"Wnt signaling pathway")

Rosiglitazone is a TZD derivative that was recently observed to improve cognition in both APP transgenic mice and AD patients [Watson et al., 2005; Pedersen et al., 2006]. It activates PPARgamma leading to increased glucose disposal rates [Jung et al., 2005] and is also neuroprotective against Abeta neurotoxicity [Inestrosa et al., 2005]. Neuroprotection may result through modulation of Wnt signaling since an increase in beta-catenin and inhibition of GSK-3beta is observed upon exposure to rosiglitazone [Inestrosa et al., 2005], although a different study has shown that activation of PPARgamma by a potent ligand leads to beta-catenin degradation [Liu and Farmer 2004]. Nonetheless, in support of the role for PPARgamma activation in neuroprotection, PPARgamma agonists have potent anti-inflammatory effects [Luna-Medina et al., 2005], inhibit microglial activation [Bernardo et al., 2005; Heneka et al., 2005] and have been shown to improve verbal memory in AD patients with T2DM, possibly in a mechanism dependent on PPARgamma activation . A recent report demonstrates that overexpression of PPARgamma in cultured cells leads to a dramatic decrease in the production of Abeta, by increasing the rate of APP degradation via ubiquitination [D'Abramo et al., 2005]. This study also showed that by decreasing Abeta secretion, PPARgamma protects the cells against H2O2-mediated necrosis [D'Abramo et al., 2005]. PubMed:19885299

p(RGD:Dkk1) negativeCorrelation bp(GOBP:"Wnt signaling pathway")

Here, we report that the Wnt antagonist Dkk-1 selectively increases tau phosphorylation in the hippocampus of aged rats at Ser199/202, Ser396/404, and Ser214 sites PubMed:24270208

a(CHEBI:curcumin) increases bp(GOBP:"Wnt signaling pathway")

Curcumin nanoparticles increase neuronal differentiation by activating the Wnt/beta-catenin pathway, involved in regulation of neurogenesis. These nanoparticles caused enhanced nuclear translocation of beta-catenin, decreased GSK-3beta levels, and increased promoter activity of the TCF/LEF and cyclin-D1. PubMed:24467380

r(HGNC:DPYSL3) positiveCorrelation bp(GOBP:"Wnt signaling pathway")

Several components in the Wnt signaling pathway, including beta-catenin and glycogen synthase kinase 3 beta, have been implied in AD pathogenesis. Here, mRNA brain levels from five-month-old tg-ArcSwe and nontransgenic mice were compared using Affymetrix microarray analysis. With surprisingly small overall changes, Wnt signaling was the most affected pathway with altered expression of nine genes in tg-ArcSwe mice. When analyzing mRNA levels of these genes in human brain, transcription factor 7-like 2 (TCF7L2) and v-myc myelocytomatosis viral oncogene homolog (MYC), were increased in Alzheimer's disease (AD) (P < .05). Furthermore, no clear differences in TCF7L2 and MYC mRNA were found in brains with frontotemporal lobar degeneration, suggesting that altered regulation of these Wnt-related genes could be specific to AD. Finally, mRNA levels of three neurogenesis markers were analyzed. Increased mRNA levels of dihydropyrimidinase-like 3 were observed in AD brain, suggesting that altered Wnt signaling pathway regulation may signify synaptic rearrangement or neurogenesis. PubMed:21234373

p(INTERPRO:"Amyloidogenic glycoprotein, intracellular domain, conserved site") directlyDecreases bp(GOBP:"Wnt signaling pathway")

Taken together, our results identify the AICD as a novel inhibitory factor of the canonical Wnt signalling pathway and suggest its regulatory role in neuronal cell proliferation and differentiation. PubMed:22613765

p(HGNC:DKK1) decreases bp(GOBP:"Wnt signaling pathway")

Although the mechanism of Abeta action in the pathogenesis of Alzheimer's disease (AD) has remained elusive, it is known to increase the expression of the antagonist of canonical wnt signalling, Dickkopf-1 (Dkk1) PubMed:23164821

Annotations
Confidence
Very High
NeuroMMSigDB
DKK1 subgraph

p(HGNC:BRAF, var(p.Val600Glu)) association bp(GOBP:"Wnt signaling pathway")

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

p(HGNC:BRAF, var(p.Val600Glu)) association bp(GOBP:"Wnt signaling pathway")

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

g(HGNC:OVOL2) decreases bp(GOBP:"Wnt signaling pathway")

OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-β-catenin complex. Strategies to increase levels of OVOL2 might be developed to reduce colorectal tumor progression and metastasis. PubMed:26619963

path(MESHD:Neoplasms) association bp(GOBP:"Wnt signaling pathway")

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

p(HGNC:CHD4) decreases bp(GOBP:"Wnt signaling pathway")

We find that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of TSGs, suggesting that their combined inhibition may be beneficial for the treatment of colon cancer. PubMed:23708667

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

path(MESHD:"Colorectal Neoplasms") negativeCorrelation bp(GOBP:"Wnt signaling pathway")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

g(HGNC:APC) association bp(GOBP:"Wnt signaling pathway")

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

p(HGNC:BRAF, var(p.Val600Glu)) association bp(GOBP:"Wnt signaling pathway")

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

bp(GOBP:"tissue morphogenesis") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"cell adhesion") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

path(MESHD:Neoplasms) association bp(GOBP:"Wnt signaling pathway")

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

g(HGNC:OVOL2) decreases bp(GOBP:"Wnt signaling pathway")

OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-β-catenin complex. Strategies to increase levels of OVOL2 might be developed to reduce colorectal tumor progression and metastasis. PubMed:26619963

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

path(MESHD:"Colorectal Neoplasms") negativeCorrelation bp(GOBP:"Wnt signaling pathway")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

p(HGNC:CHD4) decreases bp(GOBP:"Wnt signaling pathway")

We find that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of TSGs, suggesting that their combined inhibition may be beneficial for the treatment of colon cancer. PubMed:23708667

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

g(HGNC:APC) association bp(GOBP:"Wnt signaling pathway")

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

p(HGNC:SOX2) directlyDecreases bp(GOBP:"Wnt signaling pathway")

Some members of the SOX family are negative regulators of the WNT-beta-catenin-TCF signaling pathway. PubMed:11891528

p(HGNC:ABCB1) association bp(GOBP:"Wnt signaling pathway")

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

Annotations
Experimental Factor Ontology (EFO)
SW 480 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
macrophage
NCBI Taxonomy Ids
9606

p(HGNC:TCF7L2) association bp(GOBP:"Wnt signaling pathway")

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

Annotations
Experimental Factor Ontology (EFO)
SW 480 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
macrophage
NCBI Taxonomy Ids
9606

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Figure 6 Notch function in cervical cancer. A theoretical model of how the tumour-suppressor properties of NOTCH1 can, in principle, be sidestepped in HPV-infected cervical cancer cells, allowing manifestation of growth-promoting properties of NOTCH1. Apart from HPV E6 and E7 proteins, cervical cancers frequently express increased levels of the phosphatidylinositol 3-kinase (PI3K) subunit p110? and ?Np63 as a result of amplification of the q26-29 locus of chromosome 3. Experiments show that Notch-induced PI3K confers resistance to anoikis in epithelial cells. Whether ERBB2 is induced by NOTCH in cervical cancer remains to be elucidated. PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
kidney cell
NCBI Taxonomy Ids
9606

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Skin
Cell Ontology (CL)
kidney cell
NCBI Taxonomy Ids
9606

bp(GOBP:"tissue morphogenesis") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

p(HGNC:CTNNB1) increases bp(GOBP:"Wnt signaling pathway")

Elimination of pathogenic beta-catenin suppressed constitutive Wingless/Wnt signaling and inhibited in vitro and in vivo tumor cell growth. PubMed:14563921

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
kidney cell
NCBI Taxonomy Ids
9606

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

Annotations
Experimental Factor Ontology (EFO)
DLD-1 cell
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon
Uberon
colon
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

path(MESHD:"Colorectal Neoplasms") negativeCorrelation bp(GOBP:"Wnt signaling pathway")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Annotations
Experimental Factor Ontology (EFO)
COLO 320DM cell
Experimental Factor Ontology (EFO)
SW403
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon, Ascending
NCBI Taxonomy Names
Crataegus azarolus
Uberon
lymph node
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

g(HGNC:NT5E) increases bp(GOBP:"Wnt signaling pathway")

CD73 activated EGFR and the beta-catenin/cyclin D1 signaling pathways through its enzyme and non-enzyme activities. All of the results confirmed that CD73 promotes the growth of human colorectal cancer cells through EGFR and the beta-catenin/cyclin D1 signaling pathway. CD73 may be used as a valuable biomarker of colorectal cancer. PubMed:26708311

p(HGNC:L1CAM) association bp(GOBP:"Wnt signaling pathway")

L1, a new target gene for Wnt/beta-catenin-TCF signaling, has been identified in the invasive front of colorectal cancer cells in vitro study. PubMed:17211730

p(HGNC:TGFB1) decreases bp(GOBP:"Wnt signaling pathway")

TCF/LEF transcription factors with the HMG3 box are implicated in the WNT signaling pathway and are antaGOBPnized by the transforming growth factor beta signaling pathway PubMed:11085512

p(HGNC:BRAF, var(p.Val600Glu)) association bp(GOBP:"Wnt signaling pathway")

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

p(HGNC:CHD4) decreases bp(GOBP:"Wnt signaling pathway")

We find that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of TSGs, suggesting that their combined inhibition may be beneficial for the treatment of colon cancer. PubMed:23708667

g(HGNC:APC) association bp(GOBP:"Wnt signaling pathway")

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

bp(GOBP:"cell adhesion") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

p(HGNC:AR) association bp(GOBP:"Wnt signaling pathway")

Beta-catenin, a promiscuous Wnt signaling member, has been studied intensively in relation to the androgen receptor (AR). PubMed:16126938

act(p(HGNC:AR), ma(tscript)) association bp(GOBP:"Wnt signaling pathway")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"cell growth") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

path(MESHD:Neoplasms) association bp(GOBP:"Wnt signaling pathway")

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

path(SDIS:"carcinoma of liver") association bp(GOBP:"Wnt signaling pathway")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Skin
Cell Ontology (CL)
kidney cell
NCBI Taxonomy Ids
9606

g(HGNC:OVOL2) decreases bp(GOBP:"Wnt signaling pathway")

OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-β-catenin complex. Strategies to increase levels of OVOL2 might be developed to reduce colorectal tumor progression and metastasis. PubMed:26619963

p(HGNC:SOX2) directlyDecreases bp(GOBP:"Wnt signaling pathway")

Some members of the SOX family are negative regulators of the WNT-beta-catenin-TCF signaling pathway. PubMed:11891528

p(HGNC:ABCB1) association bp(GOBP:"Wnt signaling pathway")

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

p(HGNC:TCF7L2) association bp(GOBP:"Wnt signaling pathway")

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

p(HGNC:NR2F1) association bp(GOBP:"Wnt signaling pathway")

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Figure 6 Notch function in cervical cancer. A theoretical model of how the tumour-suppressor properties of NOTCH1 can, in principle, be sidestepped in HPV-infected cervical cancer cells, allowing manifestation of growth-promoting properties of NOTCH1. Apart from HPV E6 and E7 proteins, cervical cancers frequently express increased levels of the phosphatidylinositol 3-kinase (PI3K) subunit p110? and ?Np63 as a result of amplification of the q26-29 locus of chromosome 3. Experiments show that Notch-induced PI3K confers resistance to anoikis in epithelial cells. Whether ERBB2 is induced by NOTCH in cervical cancer remains to be elucidated. PubMed:14570040

act(p(SFAM:"NOTCH Family"), ma(tscript)) decreases bp(GOBP:"Wnt signaling pathway")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

bp(GOBP:"tissue morphogenesis") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

p(HGNC:CTNNB1) increases bp(GOBP:"Wnt signaling pathway")

Elimination of pathogenic beta-catenin suppressed constitutive Wingless/Wnt signaling and inhibited in vitro and in vivo tumor cell growth. PubMed:14563921

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Annotations
Experimental Factor Ontology (EFO)
COLO 320DM cell
Experimental Factor Ontology (EFO)
SW403

path(MESHD:"Colorectal Neoplasms") association bp(GOBP:"Wnt signaling pathway")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

g(HGNC:NT5E) increases bp(GOBP:"Wnt signaling pathway")

CD73 activated EGFR and the beta-catenin/cyclin D1 signaling pathways through its enzyme and non-enzyme activities. All of the results confirmed that CD73 promotes the growth of human colorectal cancer cells through EGFR and the beta-catenin/cyclin D1 signaling pathway. CD73 may be used as a valuable biomarker of colorectal cancer. PubMed:26708311

p(HGNC:L1CAM) association bp(GOBP:"Wnt signaling pathway")

L1, a new target gene for Wnt/beta-catenin-TCF signaling, has been identified in the invasive front of colorectal cancer cells in vitro study. PubMed:17211730

p(HGNC:TGFB1) decreases bp(GOBP:"Wnt signaling pathway")

TCF/LEF transcription factors with the HMG3 box are implicated in the WNT signaling pathway and are antaGOBPnized by the transforming growth factor beta signaling pathway PubMed:11085512

bp(GOBP:"cell adhesion") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

p(HGNC:AR) association bp(GOBP:"Wnt signaling pathway")

Beta-catenin, a promiscuous Wnt signaling member, has been studied intensively in relation to the androgen receptor (AR). PubMed:16126938

act(p(HGNC:AR), ma(tscript)) association bp(GOBP:"Wnt signaling pathway")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"cell growth") association bp(GOBP:"Wnt signaling pathway")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

path(SDIS:"carcinoma of liver") association bp(GOBP:"Wnt signaling pathway")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

g(HGNC:OVOL2) decreases bp(GOBP:"Wnt signaling pathway")

OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-β-catenin complex. Strategies to increase levels of OVOL2 might be developed to reduce colorectal tumor progression and metastasis. PubMed:26619963

p(HGNC:APP) association bp(GOBP:"Wnt signaling pathway")

These findings confirm the previously reported involvement of APP in Wnt-PCP signalling, and identify a new role of APP in Wnt-β-catenin signalling. Expression of APP did not alter the specificity of pathway activation by Wnt3a and Wnt5a, which selectively activated Wnt-β-catenin and Wnt-PCP signalling, respectively. PubMed:30232325

composite(p(HGNC:APP), p(HGNC:DKK1)) association bp(GOBP:"Wnt signaling pathway")

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599 ng/ mL from 1405 ng/mL. These data suggest that APP can enhance the potency of Dkk1 to modulate Wnt signalling. PubMed:30232325

p(HGNC:DKK1) association bp(GOBP:"Wnt signaling pathway")

As the Wnt signalling modulator Dkk1 has been shown to be central in Aβ synaptotoxicity, we assessed the effects of APP on Dkk1-mediated modulation of canonical and non-canonical signalling activity. Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122 ng/mL from 173 ng/mLin the absence of APP. PubMed:30232325

bp(GOBP:"synapse organization") association bp(GOBP:"Wnt signaling pathway")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

p(HGNC:APP) association bp(GOBP:"Wnt signaling pathway")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

composite(p(HGNC:APP), p(HGNC:DKK1)) association bp(GOBP:"Wnt signaling pathway")

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599 ng/ mL from 1405 ng/mL. These data suggest that APP can enhance the potency of Dkk1 to modulate Wnt signalling. PubMed:30232325

bp(GOBP:"synapse organization") association bp(GOBP:"Wnt signaling pathway")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

p(HGNC:DKK1) association bp(GOBP:"Wnt signaling pathway")

As the Wnt signalling modulator Dkk1 has been shown to be central in Aβ synaptotoxicity, we assessed the effects of APP on Dkk1-mediated modulation of canonical and non-canonical signalling activity. Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122 ng/mL from 173 ng/mLin the absence of APP. PubMed:30232325

p(HGNC:APP) association bp(GOBP:"Wnt signaling pathway")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

Out-Edges 113

bp(GOBP:"Wnt signaling pathway") association bp(MESHPP:"Neuronal Plasticity")

In particular we found that stress and antidepressant treatment affected intracellular cascades like growth factor receptor signaling, G-protein-coupled receptor signaling, and Wnt signaling - processes involved in the neuroplastic changes observed during the progression of depression and antidepressant treatment. PubMed:24339877

bp(GOBP:"Wnt signaling pathway") positiveCorrelation path(MESHD:Neoplasms)

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
breast
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

bp(GOBP:"Wnt signaling pathway") positiveCorrelation path(MESHD:Neoplasms)

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

bp(GOBP:"Wnt signaling pathway") positiveCorrelation p(HGNC:CCND1)

Increased Cyclin D1 levels in breast cancer cell lines and tumors have been correlated with increased β-catenin accumulation and constitutive Wnt signaling (Lin et al., 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Stress Disorders, Traumatic")

Differentially regulated transcripts in the AY, HC and MPFC across four time points were significantly associated with inflammatory pathways (TNF-α, IFN-γ, IL-6, chemokine, and TLR signaling and NF-κB transcriptional activities), as well as other important signaling pathways such as histone modifications, oxidative stress, neuronal growth factors, and WNT, NOTCH, β-catenin and cyclic AMP signaling pathways (Figure 3a). PubMed:28534873

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Stress Disorders, Traumatic")

Differentially regulated transcripts in the AY, HC and MPFC across four time points were significantly associated with inflammatory pathways (TNF-α, IFN-γ, IL-6, chemokine, and TLR signaling and NF-κB transcriptional activities), as well as other important signaling pathways such as histone modifications, oxidative stress, neuronal growth factors, and WNT, NOTCH, β-catenin and cyclic AMP signaling pathways (Figure 3a). PubMed:28534873

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

bp(GOBP:"Wnt signaling pathway") negativeCorrelation path(MESHD:"Colorectal Neoplasms")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

bp(GOBP:"Wnt signaling pathway") association g(HGNC:APC)

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"brain development")

Alzheimer's disease (AD) is a neurodegenerative disease with progressive dementia accompanied by three main structural changes in the brain: diffuse loss of neurons; intracellular protein deposits termed neurofibrillary tangles (NFT) and extracellular protein deposits termed amyloid or senile plaques, surrounded by dystrophic neurites. Recent studies have suggested that the trafficking process of membrane associated proteins is modulated by the FAD-linked presenilin (PS) proteins, and that amyloid beta-peptide deposition may be initiated intracellularly, through the secretory pathway. Current hypotheses concerning presenilin function are based upon its cellular localization and its putative interaction as macromolecular complexes with the cell-adhesion/signaling beta-catenin molecule and the glycogen synthase kinase 3beta (GSK-3beta) enzyme. Developmental studies have shown that PS proteins function as components in the Notch signal transduction cascade and that beta-catenin and GSK-3beta are transducers of the Wnt signaling pathway. Both pathways are thought to have an important role in brain development, and they have been connected through Dishevelled (Dvl) protein, a known transducer of the Wnt signaling pathway. In addition to a review of the current state of research on the subject, we present a cell signaling model in which a sustained loss of function of Wnt signaling components would trigger a series of misrecognition events, determining the onset and development of AD. PubMed:10967351

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"brain development")

The Wnt signaling pathway plays a crucial role in the proper development and maintenance of brain and bone structure and function. PubMed:26880631

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"brain development")

Growing evidence indicates that wingless-type (Wnt) signaling plays an important role in neuronal development, synapse formation and synaptic plasticity. PubMed:26032671

bp(GOBP:"Wnt signaling pathway") positiveCorrelation r(HGNC:DPYSL3)

Several components in the Wnt signaling pathway, including beta-catenin and glycogen synthase kinase 3 beta, have been implied in AD pathogenesis. Here, mRNA brain levels from five-month-old tg-ArcSwe and nontransgenic mice were compared using Affymetrix microarray analysis. With surprisingly small overall changes, Wnt signaling was the most affected pathway with altered expression of nine genes in tg-ArcSwe mice. When analyzing mRNA levels of these genes in human brain, transcription factor 7-like 2 (TCF7L2) and v-myc myelocytomatosis viral oncogene homolog (MYC), were increased in Alzheimer's disease (AD) (P < .05). Furthermore, no clear differences in TCF7L2 and MYC mRNA were found in brains with frontotemporal lobar degeneration, suggesting that altered regulation of these Wnt-related genes could be specific to AD. Finally, mRNA levels of three neurogenesis markers were analyzed. Increased mRNA levels of dihydropyrimidinase-like 3 were observed in AD brain, suggesting that altered Wnt signaling pathway regulation may signify synaptic rearrangement or neurogenesis. PubMed:21234373

bp(GOBP:"Wnt signaling pathway") increases g(HGNC:FOS)

Only one of these common genes, CCND1 (cyclin D1), is a known canonical wnt target,32 with the remaining four encoding transcription factors: EGR1 (early growth response-1), NAB2 (Ngfi-A-binding protein-2), KLF10 (Krüppel-like factor-10) and FOS (FBJ murine osteosarcoma viral oncogene homologue). We confirmed the induction of these genes by both Abeta25-35 and by Dkk1 using qRT-PCR PubMed:23164821

bp(GOBP:"Wnt signaling pathway") association a(CHEBI:rosiglitazone)

Rosiglitazone is a TZD derivative that was recently observed to improve cognition in both APP transgenic mice and AD patients [Watson et al., 2005; Pedersen et al., 2006]. It activates PPARgamma leading to increased glucose disposal rates [Jung et al., 2005] and is also neuroprotective against Abeta neurotoxicity [Inestrosa et al., 2005]. Neuroprotection may result through modulation of Wnt signaling since an increase in beta-catenin and inhibition of GSK-3beta is observed upon exposure to rosiglitazone [Inestrosa et al., 2005], although a different study has shown that activation of PPARgamma by a potent ligand leads to beta-catenin degradation [Liu and Farmer 2004]. Nonetheless, in support of the role for PPARgamma activation in neuroprotection, PPARgamma agonists have potent anti-inflammatory effects [Luna-Medina et al., 2005], inhibit microglial activation [Bernardo et al., 2005; Heneka et al., 2005] and have been shown to improve verbal memory in AD patients with T2DM, possibly in a mechanism dependent on PPARgamma activation . A recent report demonstrates that overexpression of PPARgamma in cultured cells leads to a dramatic decrease in the production of Abeta, by increasing the rate of APP degradation via ubiquitination [D'Abramo et al., 2005]. This study also showed that by decreasing Abeta secretion, PPARgamma protects the cells against H2O2-mediated necrosis [D'Abramo et al., 2005]. PubMed:19885299

bp(GOBP:"Wnt signaling pathway") increases g(HGNC:KLF10)

Only one of these common genes, CCND1 (cyclin D1), is a known canonical wnt target,32 with the remaining four encoding transcription factors: EGR1 (early growth response-1), NAB2 (Ngfi-A-binding protein-2), KLF10 (Krüppel-like factor-10) and FOS (FBJ murine osteosarcoma viral oncogene homologue). We confirmed the induction of these genes by both Abeta25-35 and by Dkk1 using qRT-PCR PubMed:23164821

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:neurogenesis)

Several components in the Wnt signaling pathway, including beta-catenin and glycogen synthase kinase 3 beta, have been implied in AD pathogenesis. Here, mRNA brain levels from five-month-old tg-ArcSwe and nontransgenic mice were compared using Affymetrix microarray analysis. With surprisingly small overall changes, Wnt signaling was the most affected pathway with altered expression of nine genes in tg-ArcSwe mice. When analyzing mRNA levels of these genes in human brain, transcription factor 7-like 2 (TCF7L2) and v-myc myelocytomatosis viral oncogene homolog (MYC), were increased in Alzheimer's disease (AD) (P < .05). Furthermore, no clear differences in TCF7L2 and MYC mRNA were found in brains with frontotemporal lobar degeneration, suggesting that altered regulation of these Wnt-related genes could be specific to AD. Finally, mRNA levels of three neurogenesis markers were analyzed. Increased mRNA levels of dihydropyrimidinase-like 3 were observed in AD brain, suggesting that altered Wnt signaling pathway regulation may signify synaptic rearrangement or neurogenesis. PubMed:21234373

bp(GOBP:"Wnt signaling pathway") increases g(HGNC:NAB2)

Only one of these common genes, CCND1 (cyclin D1), is a known canonical wnt target,32 with the remaining four encoding transcription factors: EGR1 (early growth response-1), NAB2 (Ngfi-A-binding protein-2), KLF10 (Krüppel-like factor-10) and FOS (FBJ murine osteosarcoma viral oncogene homologue). We confirmed the induction of these genes by both Abeta25-35 and by Dkk1 using qRT-PCR PubMed:23164821

bp(GOBP:"Wnt signaling pathway") negativeCorrelation p(RGD:Dkk1)

Here, we report that the Wnt antagonist Dkk-1 selectively increases tau phosphorylation in the hippocampus of aged rats at Ser199/202, Ser396/404, and Ser214 sites PubMed:24270208

bp(GOBP:"Wnt signaling pathway") association p(HGNC:CTNNB1)

Rosiglitazone is a TZD derivative that was recently observed to improve cognition in both APP transgenic mice and AD patients [Watson et al., 2005; Pedersen et al., 2006]. It activates PPARgamma leading to increased glucose disposal rates [Jung et al., 2005] and is also neuroprotective against Abeta neurotoxicity [Inestrosa et al., 2005]. Neuroprotection may result through modulation of Wnt signaling since an increase in beta-catenin and inhibition of GSK-3beta is observed upon exposure to rosiglitazone [Inestrosa et al., 2005], although a different study has shown that activation of PPARgamma by a potent ligand leads to beta-catenin degradation [Liu and Farmer 2004]. Nonetheless, in support of the role for PPARgamma activation in neuroprotection, PPARgamma agonists have potent anti-inflammatory effects [Luna-Medina et al., 2005], inhibit microglial activation [Bernardo et al., 2005; Heneka et al., 2005] and have been shown to improve verbal memory in AD patients with T2DM, possibly in a mechanism dependent on PPARgamma activation . A recent report demonstrates that overexpression of PPARgamma in cultured cells leads to a dramatic decrease in the production of Abeta, by increasing the rate of APP degradation via ubiquitination [D'Abramo et al., 2005]. This study also showed that by decreasing Abeta secretion, PPARgamma protects the cells against H2O2-mediated necrosis [D'Abramo et al., 2005]. PubMed:19885299

bp(GOBP:"Wnt signaling pathway") regulates p(HGNC:CTNNB1, pmod(Ub))

In the Wnt/beta-catenin cascade, signaling events converge on the regulation of ubiquitin-mediated degradation of the crucial transcriptional regulator beta-catenin. PubMed:20930545

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"regulation of bone development")

The Wnt signaling pathway plays a crucial role in the proper development and maintenance of brain and bone structure and function. PubMed:26880631

bp(GOBP:"Wnt signaling pathway") increases g(HGNC:EGR1)

Only one of these common genes, CCND1 (cyclin D1), is a known canonical wnt target,32 with the remaining four encoding transcription factors: EGR1 (early growth response-1), NAB2 (Ngfi-A-binding protein-2), KLF10 (Krüppel-like factor-10) and FOS (FBJ murine osteosarcoma viral oncogene homologue). We confirmed the induction of these genes by both Abeta25-35 and by Dkk1 using qRT-PCR PubMed:23164821

bp(GOBP:"Wnt signaling pathway") decreases path(MESHD:"Alzheimer Disease")

Alzheimer's disease (AD) is a neurodegenerative disease with progressive dementia accompanied by three main structural changes in the brain: diffuse loss of neurons; intracellular protein deposits termed neurofibrillary tangles (NFT) and extracellular protein deposits termed amyloid or senile plaques, surrounded by dystrophic neurites. Recent studies have suggested that the trafficking process of membrane associated proteins is modulated by the FAD-linked presenilin (PS) proteins, and that amyloid beta-peptide deposition may be initiated intracellularly, through the secretory pathway. Current hypotheses concerning presenilin function are based upon its cellular localization and its putative interaction as macromolecular complexes with the cell-adhesion/signaling beta-catenin molecule and the glycogen synthase kinase 3beta (GSK-3beta) enzyme. Developmental studies have shown that PS proteins function as components in the Notch signal transduction cascade and that beta-catenin and GSK-3beta are transducers of the Wnt signaling pathway. Both pathways are thought to have an important role in brain development, and they have been connected through Dishevelled (Dvl) protein, a known transducer of the Wnt signaling pathway. In addition to a review of the current state of research on the subject, we present a cell signaling model in which a sustained loss of function of Wnt signaling components would trigger a series of misrecognition events, determining the onset and development of AD. PubMed:10967351

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"stem cell division")

Dysregulation of Wnt, Notch, Hedgehog and/or TGF-β signaling pathways that are involved in proliferation and maintenance of CSCs leads to the development of CRC. This review focuses on the signaling pathways relevant for CRC to understand the mechanisms leading to tumor progression and therapy resistance, which may help in the development of therapeutic strategies for CRC. PubMed:22866952

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

bp(GOBP:"Wnt signaling pathway") association p(HGNC:BRAF, var(p.Val600Glu))

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
colorectal cancer
MeSH
Neoplasms

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"stem cell division")

Dysregulation of Wnt, Notch, Hedgehog and/or TGF-β signaling pathways that are involved in proliferation and maintenance of CSCs leads to the development of CRC. This review focuses on the signaling pathways relevant for CRC to understand the mechanisms leading to tumor progression and therapy resistance, which may help in the development of therapeutic strategies for CRC. PubMed:22866952

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
Caco-2
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association p(HGNC:BRAF, var(p.Val600Glu))

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association g(HGNC:APC)

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

bp(GOBP:"Wnt signaling pathway") negativeCorrelation path(MESHD:"Colorectal Neoplasms")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"stem cell division")

Dysregulation of Wnt, Notch, Hedgehog and/or TGF-β signaling pathways that are involved in proliferation and maintenance of CSCs leads to the development of CRC. This review focuses on the signaling pathways relevant for CRC to understand the mechanisms leading to tumor progression and therapy resistance, which may help in the development of therapeutic strategies for CRC. PubMed:22866952

bp(GOBP:"Wnt signaling pathway") association p(HGNC:BRAF, var(p.Val600Glu))

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"cell adhesion")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") directlyIncreases r(HGNC:TDGF1)

The present study demonstrates a direct transcriptional regulation of the short form CR-1 expression by the canonical Wnt signaling pathway through an intronic-exonic enhancer element, containing three tandem TCF/LEF binding sites within the CR-1 gene. PubMed:17291450

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association g(HGNC:APC)

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") negativeCorrelation path(MESHD:"Colorectal Neoplasms")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"adipose tissue development")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"tissue morphogenesis")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"regulation of branching involved in mammary gland duct morphogenesis")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

Appears in Networks:
Annotations
MeSH
Extracellular Matrix
Experimental Factor Ontology (EFO)
COS-1 cell
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"tissue morphogenesis")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:AR)

Beta-catenin, a promiscuous Wnt signaling member, has been studied intensively in relation to the androgen receptor (AR). PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association act(p(HGNC:AR), ma(tscript))

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:BRAF, var(p.Val600Glu))

In this study we report a molecular profile for a BRAF oncogenic mutation BRAFV600E in colon using the Illumina 45,000 gene microarray. Key differentially expressed genes have been identified from the array analysis further verified by qPCR analysis. Ingenuity pathway analysis such as microsatellite instability, kinase signalling, apoptosis, WNT and Integrin signalling is presented. MutBRAF transforms cells through cross talk with developmental pathways Hedgehog and Wnt, as well as by deregulation of colorectal cancer related kinase pathways, like PI3K. PubMed:22515520

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association path(SDIS:"carcinoma of liver")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Skin
Cell Ontology (CL)
kidney cell
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association p(HGNC:L1CAM)

L1, a new target gene for Wnt/beta-catenin-TCF signaling, has been identified in the invasive front of colorectal cancer cells in vitro study. PubMed:17211730

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"cell adhesion")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"cell growth")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"stem cell division")

Dysregulation of Wnt, Notch, Hedgehog and/or TGF-β signaling pathways that are involved in proliferation and maintenance of CSCs leads to the development of CRC. This review focuses on the signaling pathways relevant for CRC to understand the mechanisms leading to tumor progression and therapy resistance, which may help in the development of therapeutic strategies for CRC. PubMed:22866952

Annotations
Experimental Factor Ontology (EFO)
Caco-2
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association g(HGNC:APC)

The tumor suppressor Adenomatous polyposis coli (APC) plays a key role in regulating the canonical Wnt signaling pathway as an essential component of the β-catenin destruction complex. PubMed:26446838

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

bp(GOBP:"Wnt signaling pathway") increases path(SDIS:"carcinoma of prostate gland")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"regulation of branching involved in mammary gland duct morphogenesis")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

Annotations
Experimental Factor Ontology (EFO)
DLD-1 cell
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon
Uberon
colon
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Potential treatment strategies include revisiting old targets such as human epidermal growth factor receptor 2, RAS, and BRAF and investigating new targets such as c-MET, the PI3 kinase, and Wnt pathways, and also the use of immune-checkpoint inhibitors. PubMed:27154421

bp(GOBP:"Wnt signaling pathway") negativeCorrelation path(MESHD:"Colorectal Neoplasms")

The Wnt/β-catenin pathway is a well-known oncogenic pathway. Its suppression has long been considered as an important challenge in treating cancer patients. PubMed:27196752

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Annotations
Experimental Factor Ontology (EFO)
COLO 320DM cell
Experimental Factor Ontology (EFO)
SW403
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon, Ascending
NCBI Taxonomy Names
Crataegus azarolus
Uberon
lymph node
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

we now know that more than 80% of sporadic colon tumors contain mutations in the Wnt and TGFβ signaling pathways. PubMed:21472043

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"cell proliferation")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:TCF7L2)

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

Annotations
Experimental Factor Ontology (EFO)
SW 480 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
macrophage
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"adipose tissue development")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:ABCB1)

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

Annotations
Experimental Factor Ontology (EFO)
SW 480 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
macrophage
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"tissue morphogenesis")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:AR)

Beta-catenin, a promiscuous Wnt signaling member, has been studied intensively in relation to the androgen receptor (AR). PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association act(p(HGNC:AR), ma(tscript))

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association path(SDIS:"carcinoma of liver")

Notch1 exerts its tumour-suppressive effect in the mouse skin partially by repressing components of the Wnt (see a) and Shh (see b) signalling pathways.Activation of both pathways has been associated with many forms of cancer.Activation of WNT signalling has been linked with colorectal cancer, hepatocellular tumours, pilomatricomas, melanomas and other types of cancer (for a review, see REF. 98).Aberrant SHH signalling has been associated with sporadic basal-cell carcinoma, medulloblastoma and rhabdomyosarcoma (for a review, see REF. 138). PubMed:14570040

bp(GOBP:"Wnt signaling pathway") association p(HGNC:L1CAM)

L1, a new target gene for Wnt/beta-catenin-TCF signaling, has been identified in the invasive front of colorectal cancer cells in vitro study. PubMed:17211730

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

The cross-regulation of Wnt/beta-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:NR2F1)

Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/beta-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/beta-catenin/Tcf cascade (theme II). PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"cell adhesion")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"cell growth")

Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") increases path(SDIS:"carcinoma of prostate gland")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"regulation of branching involved in mammary gland duct morphogenesis")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Malfunctioning of the adenomatous polyposis coli (APC)/β-catenin signaling pathway is both an early and common event in sporadic colorectal cancer./ PubMed:22539608

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Moreover, PARP family enzyme assays showed that K-756 is a selective TNKS inhibitor. K-756 inhibited the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. PubMed:27196752

Annotations
Experimental Factor Ontology (EFO)
COLO 320DM cell
Experimental Factor Ontology (EFO)
SW403

bp(GOBP:"Wnt signaling pathway") association path(MESHD:"Colorectal Neoplasms")

Mutations of mismatch repair genes, e.g., MSH3 and MSH6, and genes in PI3K, WNT, TGF-β and BMP signaling (but not in TP53 signaling) were significantly involved in high-methylation CRC compared with adenoma, suggesting importance of abrogation of these genes in serrated pathway. PubMed:26510091

bp(GOBP:"Wnt signaling pathway") increases a(MeSH:"Neoplastic Stem Cells")

Indeed, Wnt signaling activity was shown to designate colon CSCs and is, therefore, an attractive target for new therapeutics. PubMed:21159886

bp(GOBP:"Wnt signaling pathway") increases bp(GOBP:"cell proliferation")

Beta-catenin acts as a coactivator of AR transcription and is also involved in co-trafficking, increasing cell proliferation, and prostate pathogenesis. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:TCF7L2)

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

bp(GOBP:"Wnt signaling pathway") directlyIncreases bp(GOBP:"adipose tissue development")

Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. Beta-catenin has been intensively studied in colorectal cancer; however, it is now evident that beta-catenin may be important in cancers of the breast, prostate, and thyroid. PubMed:16126938

bp(GOBP:"Wnt signaling pathway") association p(HGNC:ABCB1)

The multidrug resistance 1 (MDRI) gene and transcription factor 4(TCF4) gene are suggested to be involved in the WNT signalling pathway PubMed:11980438

bp(GOBP:"Wnt signaling pathway") increases a(MeSH:"Neoplastic Stem Cells")

Indeed, Wnt signaling activity was shown to designate colon CSCs and is, therefore, an attractive target for new therapeutics. PubMed:21159886

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

bp(GOBP:"Wnt signaling pathway") association p(HGNC:APP)

These findings confirm the previously reported involvement of APP in Wnt-PCP signalling, and identify a new role of APP in Wnt-β-catenin signalling. Expression of APP did not alter the specificity of pathway activation by Wnt3a and Wnt5a, which selectively activated Wnt-β-catenin and Wnt-PCP signalling, respectively. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association p(HGNC:APP)

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association p(HGNC:DKK1)

As the Wnt signalling modulator Dkk1 has been shown to be central in Aβ synaptotoxicity, we assessed the effects of APP on Dkk1-mediated modulation of canonical and non-canonical signalling activity. Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122 ng/mL from 173 ng/mLin the absence of APP. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"synapse organization")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association composite(p(HGNC:APP), p(HGNC:DKK1))

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599 ng/ mL from 1405 ng/mL. These data suggest that APP can enhance the potency of Dkk1 to modulate Wnt signalling. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association p(HGNC:APP)

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association p(HGNC:DKK1)

As the Wnt signalling modulator Dkk1 has been shown to be central in Aβ synaptotoxicity, we assessed the effects of APP on Dkk1-mediated modulation of canonical and non-canonical signalling activity. Overexpression of APP enhanced the inhibitory effects of Dkk1 on Wnt3a induced Wnt-β-catenin signalling, counteracting the enhanced activity resulting from APP overexpression and reducing the IC50 of Dkk1 to 122 ng/mL from 173 ng/mLin the absence of APP. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association bp(GOBP:"synapse organization")

An involvement of APP in Wnt signalling, which regulates synapse formation and stability, raises the question of whether familial AD mutations in APP may impact the activity of APP in Wnt signalling. PubMed:30232325

bp(GOBP:"Wnt signaling pathway") association composite(p(HGNC:APP), p(HGNC:DKK1))

In contrast, the stimulatory effects of Dkk1 on WntPCP signalling induced by Wnt5a were enhanced by APP overexpression, decreasing the EC50 of Dkk1 to 599 ng/ mL from 1405 ng/mL. These data suggest that APP can enhance the potency of Dkk1 to modulate Wnt signalling. PubMed:30232325

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