HGF/c-Met Cancer Research Results

HGF/c-Met, met proto-oncogene (hepatocyte growth factor receptor): Click to Expand ⟱

Source: CGL-Driver Genes

Type: Oncogene

Hepatocyte growth factor (HGF) and its high-affinity receptor, mesenchymal epithelial transition factor (c-Met), are closely related to the onset, progression, and metastasis of multiple tumors. The HGF/c-Met axis is involved in cell proliferation, movement, differentiation, invasion, angiogenesis, and apoptosis by activating multiple downstream signaling pathways.
HGF (Hepatocyte Growth Factor) and its receptor c-Met play significant roles in various biological processes, including cell growth, motility, and differentiation. Their involvement in cancer has been extensively studied, as the HGF/c-Met signaling pathway is often dysregulated in many types of tumors
: The HGF/c-Met pathway can promote tumor cell proliferation and survival. When HGF binds to c-Met, it activates several downstream signaling pathways, including the PI3K/Akt and MAPK pathways, which are crucial for cell survival and growth.
c-Met is associated with increased invasive and metastatic potential of cancer cells. The activation of this pathway can enhance the motility of cancer cells, allowing them to invade surrounding tissues and spread to distant sites.
Tumors that overexpress c-Met may evade the effects of treatment, leading to poor patient outcomes.

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

luteolin could act as a novel <span class="wphighlight">HGF/c-Met</span> inhibitor

FASN↓, cMET↓, HGF/c-Met↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,

Cell Death ⓘ

HGF/c-Met↓, 1,

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,
Total Targets: 3

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: HGF/c-Met, met proto-oncogene (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