The key genes MET, HGF and MMP7 reported together with MACC1 showed significant positive correlations with MACC1 in more than half of the cancer types included in the big data analysis.
<b>Introduction</b>: The HGF/MET axis is a key therapeutic pathway in cancer; it is aberrantly activated because of mutations, fusions, amplification or aberrant ligand production.
The association between HGF and miR‑200a was associated with the degree of tumor malignancy and cell migration and invasion. miR‑200a negatively regulated HGF expression by targeting the 3'‑untranslated region of the HGF mRNA. miR‑200a overexpression induced HGF downregulation, decreased NSCLC cell migration and invasion, promoted apoptosis, and decreased cell survival in A549 and H1299 cells in response to ionizing radiation.
Our data collectively demonstrate that cancer cell derived sEVs contribute to recipient cell metastasis through promoting HGF/c-Met pathway, which are potential targets for the prevention and treatment of cancer metastasis.
To test the effect of HGF neutralization with antibody on anti-cancer T cell immunity, we generated surrogate antibodies that are reactive to the mouse homologue of the epitope targeted by YYB-101.
MET tyrosine kinase receptor [MET, c-MET, hepatocyte growth factor (HGF) receptor] pathway activation is associated with the appearance of several hallmarks of cancer.
In sum, the SPINT2 gene is epigenetically silenced or downregulated in human cancers, altering the balance of HGF activation/inhibition ratio, which contributes to cancer development and progression.
However, we found that murine HGF is not completely inactive on human airway epithelial cells or cancer cell lines but stimulates the phosphorylation of GRB2-associated-binding protein 2 (GAB2) and signal transducer and activator of transcription 6 (STAT6).
In this review, we discuss how, and to what extent HGF contributes to IR and diabetes pathophysiology, as well as its role in cancer which is more prevalent in obesity and diabetes.
Its presence in tumor microenvironment could foster among other the expression of VEGF, HGF, Met protoncogene which induces degradation of the extracellular matrix and TWIST gene, which is in turn involved in a mechanism of cancer cell metastasis called epithelial-mesenchimal transition(EMT).
Different therapeutic approaches targeting the HGF/c-Met signalling pathway are under development for targeted cancer therapy, among which small molecule inhibitors of c-Met kinase constitute the largest effort within the pharmaceutical industry.
Both tested compounds attenuated HGF-mediated proliferation across various established c-Met<sup>+</sup> cancer cell lines and altered cell cycle distribution accompanied by apoptosis induction.
Carcinoma-associated fibroblasts (CAFs) are dominant components of the tumor microenvironment (TME) that promote the development, progression and metastasis of cancer. c-Met is a receptor of the hepatocyte growth factor (HGF), which is involved in lymphangiogenesis.
Circulating HGF levels were significantly associated with the stage of cancer at diagnosis (P=0.044), but lacked a significant association with lymph node status (P=0.194).
Hepatocyte growth factor (HGF)/MET signaling is implicated in the development of colorectal cancer (CRC) and possesses therapeutic value for various types of cancer.
The growth and motility factor Hepatocyte Growth Factor/Scatter Factor (HGF/SF) and its receptor, the product of the MET proto-oncogene, promote invasion and metastasis of tumor cells and have been considered potential targets for cancer therapy.