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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.
Tyrosine kinase inhibition
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