Target intelligence / Profile preview

c-Met Proto-Oncogene Receptor Tyrosine Kinase (c-Met)

Target
c-Met
Molecular classification
Receptor Tyrosine Kinase (RTK)
01

Overview

c-Met, also known as MET proto-oncogene, is a receptor tyrosine kinase (RTK) that serves as the high-affinity receptor for hepatocyte growth factor (HGF). Upon HGF binding, c-Met undergoes dimerization and autophosphorylation, activating downstream signaling pathways involved in cell proliferation, survival, motility, and invasion. Aberrant activation of c-Met, through mutation, amplification, or overexpression, is implicated in tumorigenesis across many cancers, making it a therapeutic target. Inhibitors targeting c-Met are under clinical investigation for various solid tumors.

Other names
MET proto-oncogeneHepatocyte Growth Factor Receptor (HGFR)Scatter Factor Receptor (SF Receptor)
02

Mechanism of action

Tyrosine kinase inhibition

03

Biological functions

Cell proliferationCell motilityCell survivalCell invasionWound healingAngiogenesisEmbryonic developmentOrganogenesis
04

Disease associations

Cancer (various solid tumors)Papillary renal cell carcinomaHepatocellular carcinomaNon-small cell lung cancer (NSCLC)Breast cancerOvarian cancerColon cancerKidney cancerThyroid cancer
05

Safety considerations

Resistance to inhibitorsOff-target effectsDevelopment of secondary malignancies
06

Interacting drugs

Crizotinib
07

Biomarkers

c-Met overexpressionMET gene amplificationMET mutations

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