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.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, ChemoSen↑, chemoP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSTs↑, *GSH↑, *TNF-α↓, *IL1β↓, *Casp3↓, *IL10↑, NRF2↓, HO-1↓, NQO1↓, GSH↓, MET↓, p‑MET↓, p‑Akt↓, HGF/c-Met↓, NF-kB↓, Bcl-2↓, SOD2↓, Casp8↑, Casp3↑, PARP↑, MAPK↓, NLRP3↓, ASC↓, Casp1↓, IL6↓, IKKα↓, p‑p65↓, p‑p38↑, MMP2↓, ICAM-1↓, EGFR↑, p‑PI3K↓, E-cadherin↓, ZO-1↑, N-cadherin↓, CLDN1↓, β-catenin/ZEB1↓, Snail↓, Vim↑, ITGB1↓, FAK↓, p‑Src↓, Rac1↓, Cdc42↓, Rho↓, PCNA↓, Tyro3↓, AXL↓, CEA↓, NSE↓, SOD↓, Catalase↓, GPx↓, GSR↓, GSTs↓, GSH↓, VitE↓, VitC↓, CYP1A1↓, cFos↑, AR↓, AIF↑, p‑STAT6↓, p‑MDM2↓, NOTCH1↓, VEGF↓, H3↓, H4↓, HDAC↓, SIRT1↓, ROS↑, DR5↑, Cyt‑c↑, p‑JNK↑, PTEN↓, mTOR↓, CD34↓, FasL↑, Fas↑, XIAP↓, p‑eIF2α↑, CHOP↑, LC3II↑, PD-1↓, STAT3↓, IL2↑, EMT↓, cachexia↓, BioAv↑, *Half-Life↝, *eff↑,
3930- PTS,    A Review of Pterostilbene Antioxidant Activity and Disease Modification
- Review, Var, NA - Review, adrenal, NA - Review, Stroke, NA
*BioAv↑, *antiOx↑, *neuroP↑, *Inflam↓, *ROS↓, *H2O2↓, *GSH↑, *GPx↑, *GSR↑, *SOD↑, TumCG↓, PTEN↑, HGF/c-Met↓, PI3K↓, Akt↓, NF-kB↓, TumMeta↓, MMP2↓, MMP9↓, Ki-67↓, Casp3↑, MMP↓, H2O2↑, ROS↑, ChemoSen↑, *cardioP↑, *CDK2↓, *CDK4↓, *cycE/CCNE↓, *cycD1/CCND1↓, *RB1↓, *PCNA↓, *CREB↑, *GABA↑, *memory↑, *IGF-1↑, *ERK↑, TIMP1↑, BAX↑, Cyt‑c↑, Diablo↑, SOD2↑,

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 ⓘ

Catalase↓, 1,   CYP1A1↓, 1,   GPx↓, 1,   GSH↓, 2,   GSR↓, 1,   GSTs↓, 1,   H2O2↑, 1,   HO-1↓, 1,   NQO1↓, 1,   NRF2↓, 1,   ROS↑, 2,   SOD↓, 1,   SOD2↓, 1,   SOD2↑, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp1↓, 1,   Casp3↑, 2,   Casp8↑, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   FasL↑, 1,   HGF/c-Met↓, 2,   p‑JNK↑, 1,   MAPK↓, 1,   p‑MDM2↓, 1,   p‑p38↑, 1,  

Transcription & Epigenetics ⓘ

H3↓, 1,   H4↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,  

DNA Damage & Repair ⓘ

PARP↑, 1,   PCNA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   cFos↑, 1,   EMT↓, 1,   HDAC↓, 1,   mTOR↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,   p‑PI3K↓, 1,   PTEN↓, 1,   PTEN↑, 1,   p‑Src↓, 1,   STAT3↓, 1,   p‑STAT6↓, 1,   TumCG↓, 1,  

Migration ⓘ

AXL↓, 1,   Cdc42↓, 1,   CEA↓, 1,   CLDN1↓, 1,   E-cadherin↓, 1,   FAK↓, 1,   ITGB1↓, 1,   Ki-67↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP2↓, 2,   MMP9↓, 1,   N-cadherin↓, 1,   Rac1↓, 1,   Rho↓, 1,   Snail↓, 1,   TIMP1↑, 1,   TumMeta↓, 1,   Tyro3↓, 1,   Vim↑, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↑, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   IL2↑, 1,   IL6↓, 1,   NF-kB↓, 2,   p‑p65↓, 1,   PD-1↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   CEA↓, 1,   EGFR↑, 1,   IL6↓, 1,   Ki-67↓, 1,   NSE↓, 1,  

Functional Outcomes ⓘ

cachexia↓, 1,   chemoP↑, 1,  
Total Targets: 103

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 2,   GSH↑, 2,   GSR↑, 1,   GSTs↑, 1,   H2O2↓, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

CREB↑, 1,  

Cell Death ⓘ

Casp3↓, 1,  

DNA Damage & Repair ⓘ

PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   RB1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   IGF-1↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 1,   IL1β↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

GABA↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 1,   Half-Life↝, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 31

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:26  Cells:%  prod#:%  Target#:186  State#:%  Dir#:1
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