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.
Scientific Papers found: Click to Expand⟱
6010- CGA,    The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review
- Review, Nor, NA
*antiOx↑, mainly shown as anti-oxidant, liver and kidney protection, anti-bacterial, anti-tumor, regulation of glucose metabolism and lipid metabolism, anti-inflammatory, protection of the nervous system,
*hepatoP↑,
*RenoP↑,
AntiTum↑,
*glucose↝,
*Inflam↓,
*neuroP↑,
*ROS↓, ↓Active oxygen (ROS) , ↓Keap1,↑Nrf2, ↑SOD, ↑CAT, ↑Glutathione Peroxidase (GSH-Px), ↑Glutathione (GSH), ↓MDA
*Keap1↓,
*NRF2↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*MDA↓,
*p‑ERK↑, ↑ERK1/2 phosphorylation
*GRP78/BiP↑, ↑Glucose regulatory protein 78 (GRP78)
*CHOP↑, ↑C/EBP homologous protein (CHOP)
*GRP94↑, ↑Glucose Regulatory Protein 94 (GRP94)
*Casp3↓, ↓Caspase-9/Caspase-3
*Casp9↓,
*HGF/c-Met↑, ↑Hepatocyte Growth Factor (HGF)
*TNF-α↓, ↓Tumor Necrosis Factor-α (TNF-α)/Interferonγ (IFN-γ)
*TLR4↓, ↓TLR4
*MAPK↓, ↓MAPK signal pathway
*IL1β↓, ↓Interleukin 1β (IL-1β)/Interleukin 6 (IL-6)
*iNOS↓, ↓Inducible Nitric Oxide Synthase (iNOS)
TCA↓, ↓Tricarboxylic acid cycle (TCA) ↓Glycolysis
Glycolysis↓,
Bcl-2↓, ↓Anti-apoptotic gene Bcl-2/Bcl-XL
BAX↑, ↑Pro-apoptotic gene Bax/Bcl-XS/Bad
MAPK↑, ↑p38 mitogen-activated protein kinase (p38 MAPK)
JNK↑, ↑c-Jun N-terminal Kinase (JNK)
CSCs↓, ↓Stem cell marker genes Nanog, POU5F1, Sox2, CD44, Oct4
Nanog↓,
SOX2↓,
CD44↓,
OCT4↓,
P53↑, ↑P53
P21↑, ↑p21
*SOD1↑, ↑CuZnSOD (SOD1)/MnSOD (SOD2)
*AGEs↓, ↓Glycosylation end products (AGEs)
*GLUT2↑, ↑Glucose Transporter 2 (GLUT2)
*HDL↑, ↑High-density lipoprotein (HDL)
*Fas↓, ↓Fatty acid synthase (FAS)
*HMG-CoA↓, ↓β-hydroxy-β-methylglutamyl-CoA (HMG-CoA) reductase
*NF-kB↓, ↑NF-κB signaling pathway
*HO-1↓, ↑Nrf2/HO-1 signaling pathway
*COX2↓, ↓Cyclooxygenase-2 (COX-2)
*TLR4↓, ↓Toll-like receptor 4 (TLR4)
*BioAv↑, One route may be immediate absorption in the stomach or upper gastrointestinal tract, and the other route may be slowly absorbed throughout the small intestine.
*BioAv↝, It indicates that the bioavailability of CGA is closely related to the metabolic capacity of the organism's gut flora
TumCP↓, CGA also inhibits the proliferation, migration, and invasion of cancer cells.
TumCMig↓,
TumCI↓,

3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, 50 Hz, 1 mT for 24/48/72 h SH-SY5Y (neuroblastoma Significantly increased ROS levels
*Ca+2↑, There is experimental proof that extremely low-frequency (ELF-MF) magnetic fields interact with Ca2+ channels, leading to increased Ca2+ efflux
*Inflam↓, PEMF stimulates the anti-inflammatory response of mesenchymal stem cells.
*Akt↓, nasopharyngeal carcinoma cell line. Potentially, these alterations were caused by inhibition of the Akt/mTOR signaling pathway
*mTOR↓,
selectivity↑, Ashdown and colleagues observed disruptions in the human lung cancer cell line after PMF (20 mT) exposure; in comparison, normal cells were insensitive to PMF
*memory↑, Ahmed and colleagues proved that PMF has an impact on the hippocampus, the brain region responsible for spatial orientation and memory acquisition.
*MMPs↑, In wound closure, epithelial cells, connective tissue cells, and immune cells, which promote collagen production, matrix metalloproteinase activity, growth factor release (e.g., VEGF, FGF, PDGF, TNF, HGF, and IL-1), and inflammatory environment pro
*VEGF↑,
*FGF↑,
*PDGF↑,
*TNF-α↑,
*HGF/c-Met↑,
*IL1↑,


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,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   TCA↓, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   JNK↑, 1,   MAPK↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   Nanog↓, 1,   OCT4↓, 1,   SOX2↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HDL↑, 1,   HO-1↓, 1,   Keap1↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   SOD1↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↝, 1,   GLUT2↑, 1,   HMG-CoA↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Casp3↓, 1,   Casp9↓, 1,   Fas↓, 1,   HGF/c-Met↑, 2,   iNOS↓, 1,   MAPK↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   GRP78/BiP↑, 1,   GRP94↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,   FGF↑, 1,   mTOR↓, 1,  

Migration ⓘ

Ca+2↑, 1,   MMPs↑, 1,   PDGF↑, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1↑, 1,   IL1β↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TLR4↓, 2,   TNF-α↓, 1,   TNF-α↑, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 47

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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:186  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page