Mesenchymal-epithelial transition factor receptor (MET)

The mesenchymal‑epithelial transition factor receptor (MET), also known as c-Met or hepatocyte growth factor receptor (HGFR), is a prototypical member of the receptor tyrosine kinase family. It is expressed primarily on epithelial cells and is activated by its ligand hepatocyte growth factor (HGF). Upon HGF binding, the receptor undergoes dimerization and autophosphorylation on specific intracellular tyrosines. This creates docking sites for various adaptor proteins that activate multiple downstream signaling cascades—including RAS/ERK/MAPK and PI3K/AKT—regulating key cellular processes such as proliferation, survival, motility/migration, morphogenesis during development, angiogenesis, tissue repair/regeneration after injury, and invasive behavior during cancer progression. Aberrant activation of MET through gene amplification/overexpression or exon 14 skipping mutations drives oncogenic transformation in several cancers. As a result, selective small molecule inhibitors targeting aberrant MET activity have been developed for clinical use against tumors harboring these alterations[4][6][8].

Other names

c-MetHepatocyte growth factor receptorHGFRProto-oncogene METMesenchymal epithelial transition factor (Met)

– Inhibition of MET tyrosine kinase activity to block downstream signaling pathways involved in tumor cell proliferation, survival, motility, and metastasis[6][8][9]. – Antagonism of ligand binding (HGF antagonists) to prevent activation of the receptor. – Antibody-mediated inhibition to block dimerization or activation.