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path(MESH:Neoplasms)

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Entity

Name
Neoplasms
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 9

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

The Biology of Proteostasis in Aging and Disease v1.0.0

Imbalances in the Hsp90 Chaperone Machinery: Implications for Tauopathies v1.0.0

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

Phosphatase: PP2A structural importance, regulation and its aberrant expression in cancer v1.0.0

PP2A and Alzheimer Disease v1.0.0

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

In-Edges 17

path(MESH:"Tobacco Use Disorder") association path(MESH:Neoplasms) View Subject | View Object

In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

a(MESH:Acetylcholine) increases path(MESH:Neoplasms) View Subject | View Object

When lung cancer arises from the airway epithelium, cell growth is stimulated by ACh or nicotine, and this growth loop may provide endogenous mitogenic signalling without any further activation PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) increases path(MESH:Neoplasms) View Subject | View Object

When lung cancer arises from the airway epithelium, cell growth is stimulated by ACh or nicotine, and this growth loop may provide endogenous mitogenic signalling without any further activation PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(HGNC:CHRNA7) association path(MESH:Neoplasms) View Subject | View Object

In addition, various studies have shown the expression of α7 nAChR (as mRNA and protein), in many different cancer cells obtained from human tumours. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

p(HGNC:CHRNA9) increases path(MESH:Neoplasms) View Subject | View Object

Si- lencing α9 nAChR expression in the tumour cells reduces their proliferation and tumorigenic potential in in vitro and in vivo assays [122]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

act(p(HGNC:HSF1)) association path(MESH:Neoplasms) View Subject | View Object

Constitutive activation of HSF1 is detrimental to cells and increased expression, and activity of HSF1 has been linked to multiple forms of cancer, highlighting the need for appropriate and balanced activation of stress response pathways as and when required throughout life (122). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

p(HGNC:STUB1) association path(MESH:Neoplasms) View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

p(HGNC:AIFM2) negativeCorrelation path(MESH:Neoplasms) View Subject | View Object

AIFM2 (aka AMID), induced 29-fold, is implicated in caspase-independent apoptosis and was found to be downregulated in a majority of human tumors (Wu et al., 2004b). PubMed:22020111

Appears in Networks:

p(HGNC:GPX3) negativeCorrelation path(MESH:Neoplasms) View Subject | View Object

GPX3, induced 20-fold, encodes an important antioxidant enzyme, glutathione peroxidase-3, found normally in plasma and kidney but underexpressed in head and neck cancers (Chen et al., 2011). PubMed:22020111

Appears in Networks:
Annotations
MeSH
Head
MeSH
Neck

a(CHEBI:"okadaic acid") increases path(MESH:Neoplasms) View Subject | View Object

Potent tumor promoter, Okadaic acid (a microbial toxin), inhibits the enzymatic activity of PP2Ac and thereby has facilitated various studies to understand the functional aspects of PP2A and other phosphatases [12]. Other than Okadaic acid, calyculin A, microcystin, cantharidin, nodularm, fostriecin and tautomycin are able to inhibit PP2A activity at different IC50 values [48]. PubMed:23454242

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a(PUBCHEM:71361092) increases path(MESH:Neoplasms) View Subject | View Object

In addition to microbial toxin, viral protein SV40 (potent oncogene) also inactivates PP2A action by binding to the AC dimer and displacing the PR56 (PP2A-B’ γ ) subunit [35]. PubMed:23454242

Appears in Networks:

p(FPLX:PPP2) association path(MESH:Neoplasms) View Subject | View Object

PP2A is an important player in many cellular functions. It controls cell metabolism by regulating the activity of the enzymes involved in glycolysis, lipid metabolism and catecholamine synthesis [8]. It also regulates various biological processes such as the cell cycle (by mediating cdc2 kinase activation), DNA replication, transcription and translation, signal transduction, cell proliferation, cytoskeleton dynamics and cell mobility and apoptosis. It has also been shown to play a role in cell transformation and cancer [9-12]. PubMed:23454242

Appears in Networks:

p(FPLX:PPP2) decreases path(MESH:Neoplasms) View Subject | View Object

PP2A is considered as a tumor suppressor and is thought to be functionally inactivated in cancer. PubMed:23454242

Appears in Networks:

act(p(FPLX:PPP2)) negativeCorrelation path(MESH:Neoplasms) View Subject | View Object

PP2A is considered as a tumor suppressor and is thought to be functionally inactivated in cancer. PubMed:23454242

Appears in Networks:

p(FPLX:PPP2) association path(MESH:Neoplasms) View Subject | View Object

So far, the most explored pathologies in which PP2A is implicated are cancer, and some viral and parasitic diseases [44]. More recently, PP2A has been investigated in FTLD linked to mutations in the tau gene [45]. PubMed:22299660

Appears in Networks:

bp(GO:"cellular protein catabolic process") negativeCorrelation path(MESH:Neoplasms) View Subject | View Object

Considering the importance of protein catabolism in maintaining cell homeostasis, it is not surprising that dysregulation of protein turnover is associated with myriad disease states such as cancer and neurodegeneration [5]. PubMed:18930136

Appears in Networks:

bp(GO:"protein oxidation") association path(MESH:Neoplasms) View Subject | View Object

Proteome oxidation and instability has been associated with ageing and the progression of several age-related diseases, including cardiovascular disorders, neu- rodegeneration, and cancer [7,95,96]. PubMed:24563850

Appears in Networks:

Out-Edges 12

path(MESH:Neoplasms) association path(MESH:"Tobacco Use Disorder") View Subject | View Object

In fact, the relationship between tobacco abuse (including smokeless) and difficulty in healing, increased susceptibility to infection (especially oral), enhanced expression of indicators of skin aging, and increased cancer risk are all well-documented (383, 452). PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Neoplasms) association p(HGNC:CHRNA7) View Subject | View Object

In addition, various studies have shown the expression of α7 nAChR (as mRNA and protein), in many different cancer cells obtained from human tumours. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

path(MESH:Neoplasms) association act(p(HGNC:HSF1)) View Subject | View Object

Constitutive activation of HSF1 is detrimental to cells and increased expression, and activity of HSF1 has been linked to multiple forms of cancer, highlighting the need for appropriate and balanced activation of stress response pathways as and when required throughout life (122). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

path(MESH:Neoplasms) association p(HGNC:STUB1) View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

path(MESH:Neoplasms) negativeCorrelation p(HGNC:AIFM2) View Subject | View Object

AIFM2 (aka AMID), induced 29-fold, is implicated in caspase-independent apoptosis and was found to be downregulated in a majority of human tumors (Wu et al., 2004b). PubMed:22020111

Appears in Networks:

path(MESH:Neoplasms) negativeCorrelation p(HGNC:GPX3) View Subject | View Object

GPX3, induced 20-fold, encodes an important antioxidant enzyme, glutathione peroxidase-3, found normally in plasma and kidney but underexpressed in head and neck cancers (Chen et al., 2011). PubMed:22020111

Appears in Networks:
Annotations
MeSH
Head
MeSH
Neck

path(MESH:Neoplasms) association p(FPLX:PPP2) View Subject | View Object

PP2A is an important player in many cellular functions. It controls cell metabolism by regulating the activity of the enzymes involved in glycolysis, lipid metabolism and catecholamine synthesis [8]. It also regulates various biological processes such as the cell cycle (by mediating cdc2 kinase activation), DNA replication, transcription and translation, signal transduction, cell proliferation, cytoskeleton dynamics and cell mobility and apoptosis. It has also been shown to play a role in cell transformation and cancer [9-12]. PubMed:23454242

Appears in Networks:

path(MESH:Neoplasms) negativeCorrelation act(p(FPLX:PPP2)) View Subject | View Object

PP2A is considered as a tumor suppressor and is thought to be functionally inactivated in cancer. PubMed:23454242

Appears in Networks:

path(MESH:Neoplasms) association p(FPLX:PPP2) View Subject | View Object

So far, the most explored pathologies in which PP2A is implicated are cancer, and some viral and parasitic diseases [44]. More recently, PP2A has been investigated in FTLD linked to mutations in the tau gene [45]. PubMed:22299660

Appears in Networks:

path(MESH:Neoplasms) negativeCorrelation bp(GO:"cellular protein catabolic process") View Subject | View Object

Considering the importance of protein catabolism in maintaining cell homeostasis, it is not surprising that dysregulation of protein turnover is associated with myriad disease states such as cancer and neurodegeneration [5]. PubMed:18930136

Appears in Networks:

path(MESH:Neoplasms) increases p(HGNCGENEFAMILY:"Small heat shock proteins") View Subject | View Object

Specifically, they have been found overexpressed in many different diseases including various types of cancer where they contribute in reducing proteotoxic stress [7]. PubMed:24563850

Appears in Networks:

path(MESH:Neoplasms) association bp(GO:"protein oxidation") View Subject | View Object

Proteome oxidation and instability has been associated with ageing and the progression of several age-related diseases, including cardiovascular disorders, neu- rodegeneration, and cancer [7,95,96]. PubMed:24563850

Appears in Networks:

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.