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Entity

Name
Neoplasm Invasiveness
Namespace
MESHD
Namespace Version
20150611
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mesh-diseases/mesh-diseases-20150601.belns

Appears in Networks 38

BEL Framework Small Corpus Document v20150611

Approximately 2000 hand curated statements drawn from 57 PubMeds.

TBI_Xu_SecondPart v1.1.2

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 8 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

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_Xu_SecondPart v1.1.3

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 8 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

TBI_Xu_SecondPart v1.1.5

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 8 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI.

TBI_Xu_SecondPart v1.1.6

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 8 pubmed articles. 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

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

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

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

colorectal cancer Knowledge Assembly - Drugs v1.0.1

colorectal cancer Knowledge Assembly with drug associations.

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

In-Edges 48

p(HGNC:IGF1) increases path(MESHD:"Neoplasm Invasiveness")

The regulation of insulin growth factor (IGF)-I-mediated cell invasion of RCC cells appears to be dependent upon PKCd inhibition by pVHL. This inhibition is mediated through a protein–protein interaction involving a domain of pVHL that shows similarity to protein kinase inhibitor (PKI), a natural inhibitor of cAMP-dependent protein kinase (PKA) [48] PubMed:15350900

Annotations
Experimental Factor Ontology (EFO)
U-937 cell
NCBI Taxonomy Ids
9606
Uberon
cardiovascular system endothelium
Cell Ontology (CL)
fibroblast
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscle, Smooth, Vascular

p(HGNC:VHL) association path(MESHD:"Neoplasm Invasiveness")

pVHL has also been implicated in tumour invasion and metastasis, which represent complex multi-step processes that require the proteolytic degradation of the basement membrane and tissue matrix, changes in cell polarity and motility, and the attachment and detachment of cells to and from the extracellular matrix (ECM) [41]. PubMed:15350900

Annotations
Experimental Factor Ontology (EFO)
U-937 cell
NCBI Taxonomy Ids
9606
Uberon
cardiovascular system endothelium
Cell Ontology (CL)
fibroblast
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscle, Smooth, Vascular

m(RGD:Mir21) regulates path(MESHD:"Neoplasm Invasiveness")

MiR-21 regulated cell survival, invasiveness and apoptosis through speci c mRNA targets that included PTEN, which was upregulated by 3.8-fold in the mouse adult brain 24 hours post-injury PubMed:29239310

m(RGD:Mir21) regulates path(MESHD:"Neoplasm Invasiveness")

MiR-21 regulated cell survival, invasiveness and apoptosis through speci c mRNA targets that included PTEN, which was upregulated by 3.8-fold in the mouse adult brain 24 hours post-injury PubMed:29239310

Appears in Networks:
Annotations
NCBI Taxonomy Ids
10090
MeSH
Cerebral Cortex
MeSH
Mitochondria
TBI_D1_CVBio_SCAI_8-3-2018
24 hours post-injury
TBI_D1_CVBio_SCAI_8-3-2018
Moderate TBI
TBI_D1_CVBio_SCAI_8-3-2018
Mild TBI (mTBI)

deg(p(HGNC:PLAU)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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

deg(p(HGNC:BRAF)) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

deg(p(HGNC:PLAUR)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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

a(CHEBI:trametinib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

p(HGNC:GSN) positiveCorrelation path(MESHD:"Neoplasm Invasiveness")

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

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

a(CHEBI:vemurafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

a(CHEBI:dabrafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

a(MESHC:"PLX 4720") decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

bp(GOBP:"cell adhesion") increases path(MESHD:"Neoplasm Invasiveness")

Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. PubMed:23865481

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
COLO-320 cell
Experimental Factor Ontology (EFO)
HT-29
Disease Ontology (DO)
colorectal cancer
MeSH
Rectal Neoplasms

deg(p(HGNC:PLAUR)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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

a(MESHC:"PLX 4720") decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

deg(p(HGNC:PLAU)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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

deg(p(HGNC:BRAF)) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

a(CHEBI:trametinib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

a(CHEBI:vemurafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

bp(GOBP:"cell adhesion") increases path(MESHD:"Neoplasm Invasiveness")

Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. PubMed:23865481

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
Experimental Factor Ontology (EFO)
COLO-320 cell
MeSH
Rectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

p(HGNC:GSN) positiveCorrelation path(MESHD:"Neoplasm Invasiveness")

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

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

a(CHEBI:dabrafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

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

deg(p(HGNC:PLAU)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

deg(p(HGNC:BRAF)) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

deg(p(HGNC:PLAUR)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

a(CHEBI:trametinib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

p(HGNC:GSN) positiveCorrelation path(MESHD:"Neoplasm Invasiveness")

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

Annotations
NCBI Taxonomy Ids
9606
Disease Ontology (DO)
colorectal cancer

a(CHEBI:vemurafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

a(CHEBI:dabrafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

a(MESHC:"PLX 4720") decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

bp(GOBP:"cell adhesion") increases path(MESHD:"Neoplasm Invasiveness")

Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. PubMed:23865481

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
COLO-320 cell
Experimental Factor Ontology (EFO)
HT-29
Disease Ontology (DO)
colorectal cancer

a(MESHC:"PLX 4720") decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

Annotations
Experimental Factor Ontology (EFO)
LoVo cell
Experimental Factor Ontology (EFO)
LOVO cell
MeSH
Intracellular Space
MeSH
Rectal 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

a(CHEBI:trametinib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

Annotations
Experimental Factor Ontology (EFO)
LoVo cell
Experimental Factor Ontology (EFO)
LOVO cell
MeSH
Intracellular Space
MeSH
Rectal 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

a(CHEBI:vemurafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

Annotations
Experimental Factor Ontology (EFO)
LoVo cell
Experimental Factor Ontology (EFO)
LOVO cell
MeSH
Intracellular Space
MeSH
Rectal 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(MESHPP:"Tumor Microenvironment") association path(MESHD:"Neoplasm Invasiveness")

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination PubMed:24741617

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Intracellular Space
MeSH
Rectal 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

deg(p(HGNC:BRAF)) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

Annotations
Experimental Factor Ontology (EFO)
LoVo cell
Experimental Factor Ontology (EFO)
LOVO cell
MeSH
Intracellular Space
MeSH
Rectal 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

a(CHEBI:dabrafenib) decreases path(MESHD:"Neoplasm Invasiveness")

Doxycyclin-inducible knockdown of endogenous B-Raf(V600E) decreases cellular motility and invasion in conventional and three-dimensional (3D) culture, whereas it promotes cell-cell contacts and induces various hallmarks of differentiated epithelia. Importantly, all these effects are recapitulated by B-Raf (PLX4720, vemurafenib, and dabrafenib) or MEK inhibitors (trametinib). PubMed:25381152

Annotations
Experimental Factor Ontology (EFO)
LoVo cell
Experimental Factor Ontology (EFO)
LOVO cell
MeSH
Intracellular Space
MeSH
Rectal 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:GSN) increases path(MESHD:"Neoplasm Invasiveness")

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

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

deg(p(HGNC:PLAUR)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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

deg(p(HGNC:PLAU)) decreases path(MESHD:"Neoplasm Invasiveness")

The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. PubMed:22927998

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:"cell adhesion") increases path(MESHD:"Neoplasm Invasiveness")

Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P < 0.001). The treatment with oxaliplatin caused major DNA cross-links in both parental cell lines; in Colo320R small amounts of DNA cross-links were still detectable, while in HT-29R not. PubMed:23865481

Annotations
Experimental Factor Ontology (EFO)
COLO-320 cell
Experimental Factor Ontology (EFO)
HT-29
MeSH
Intracellular Space
MeSH
Rectal 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

a(CHEMBLID:CHEMBL458997) decreases path(MESHD:"Neoplasm Invasiveness")

CONCLUSIONS: Our data show inefficiency of Cetuximab and AIIB2 on top of radiochemotherapy. The functions of KRAS and BRAF in therapy resistance remain unanswered and warrant further preclinical molecular-driven investigations. One promising approach might be β1 integrin targeting for reducing metastatic CRC cell spread. PubMed:26096850

Annotations
Experimental Factor Ontology (EFO)
HT-29
Experimental Factor Ontology (EFO)
DLD1
MeSH
Intracellular Space
MeSH
Gastrointestinal 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

m(HGNC:MIR17) increases path(MESHD:"Neoplasm Invasiveness")

Overexpression of miR-17-5p promoted COLO205 cell invasiveness. PubMed:24912422

Annotations
Experimental Factor Ontology (EFO)
COLO205
MeSH
Chromatin
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

bp(MESHPP:"Tumor Microenvironment") association path(MESHD:"Neoplasm Invasiveness")

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination PubMed:24741617

p(HGNC:GSN) increases path(MESHD:"Neoplasm Invasiveness")

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

a(CHEMBLID:CHEMBL458997) decreases path(MESHD:"Neoplasm Invasiveness")

CONCLUSIONS: Our data show inefficiency of Cetuximab and AIIB2 on top of radiochemotherapy. The functions of KRAS and BRAF in therapy resistance remain unanswered and warrant further preclinical molecular-driven investigations. One promising approach might be β1 integrin targeting for reducing metastatic CRC cell spread. PubMed:26096850

Annotations
Experimental Factor Ontology (EFO)
HT-29
Experimental Factor Ontology (EFO)
DLD1
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

m(HGNC:MIR17) increases path(MESHD:"Neoplasm Invasiveness")

Overexpression of miR-17-5p promoted COLO205 cell invasiveness. PubMed:24912422

Out-Edges 6

path(MESHD:"Neoplasm Invasiveness") association p(HGNC:VHL)

pVHL has also been implicated in tumour invasion and metastasis, which represent complex multi-step processes that require the proteolytic degradation of the basement membrane and tissue matrix, changes in cell polarity and motility, and the attachment and detachment of cells to and from the extracellular matrix (ECM) [41]. PubMed:15350900

Annotations
Experimental Factor Ontology (EFO)
U-937 cell
NCBI Taxonomy Ids
9606
Uberon
cardiovascular system endothelium
Cell Ontology (CL)
fibroblast
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscle, Smooth, Vascular

path(MESHD:"Neoplasm Invasiveness") positiveCorrelation p(HGNC:GSN)

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

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

path(MESHD:"Neoplasm Invasiveness") positiveCorrelation p(HGNC:GSN)

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

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

path(MESHD:"Neoplasm Invasiveness") positiveCorrelation p(HGNC:GSN)

Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells PubMed:22927998

Annotations
NCBI Taxonomy Ids
9606
Disease Ontology (DO)
colorectal cancer

path(MESHD:"Neoplasm Invasiveness") association bp(MESHPP:"Tumor Microenvironment")

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination PubMed:24741617

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Intracellular Space
MeSH
Rectal 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

path(MESHD:"Neoplasm Invasiveness") association bp(MESHPP:"Tumor Microenvironment")

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination PubMed:24741617

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.