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c-Met/HGF pathway in HNSCC. Pro-HGF is released by TAFs and is degraded by cell surface matriptase, allowing the dimer molecule to activate the c-Met binding site. Following activation, c-Met proceeds through phosphorylation and attracts intermediary molecules Gab1 and Grb2, which then attract oncogene molecules STAT3, Ras/Raf, PI3K, and SHP2 starting regulatory pathways that induce dissemination, motility, and infiltration.
