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EGFR and c-MET have in common similar downstream pathways: MAPK (RAS/Rapidly accelerating fibrosarcoma (RAF)/ MAP kinase kinases (MEK)/ERK) and PI3K/AKT/mechanistic target of rapamycin (mTOR)

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these proteases degrade extracellular matrix (ECM) components, which facilitates cancer cell invasion, and cleave cell membrane-bound or ECM-associated precursor forms of many growth factors, thereby activating them and increasing their bioavailability in the tumour microenvironment