cMET Cancer Research Results

cMET, cellular hepatocyte growth factor receptor: Click to Expand ⟱
Source:
Type:
c-MET, also known as the hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that plays a crucial role in various cellular processes, including cell proliferation, survival, migration, and differentiation. It is activated by its ligand, hepatocyte growth factor (HGF). Dysregulation of the c-MET signaling pathway has been implicated in several types of cancer.

c-Met is often overexpressed or mutated in cancer and is associated with poor prognosis, increased metastasis, and resistance to therapies.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
1200- LT,    Inhibition of Fatty Acid Synthase by Luteolin Post-Transcriptionally Downregulates c-Met Expression Independent of Proteosomal/Lysosomal Degradation
- in-vitro, Pca, DU145
FASN↓, cMET↓, HGF/c-Met↓,
89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
PI3K/Akt↓, cMET↓, Casp3↑, Casp9↑, MMP↓, ChemoSen↑, ROS↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,   PI3K/Akt↓, 1,  

Cell Death ⓘ

Casp3↑, 1,   Casp9↑, 1,   HGF/c-Met↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: cMET, cellular hepatocyte growth factor receptor
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:22  Cells:%  prod#:%  Target#:484  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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