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MET is a well described proto-oncogene. It was first identified in the 1980s, and its ligand, hepatocyte growth factor (HGF), was later identified in the early 1990s. MET is activated when HGF binds to the receptor, inducing homodimerization and phosphorylation of intracellular tyrosine residues. Various cytoplasmic effector proteins, including GAB1, GRB2, phospholipase C, and SRC are subsequently recruited, activating the downstream RAF/ERK/MAPK, PI3K/AKT, Wnt/β-catenin, and STAT signaling pathways. After activation, MET is internalized through endocytosis and is either recycled to the plasma membrane or degraded. Depending on the cellular context, these downstream pathways can drive cell proliferation, survival, migration, motility, invasion, angiogenesis, epithelial-to-mesenchymal transition (EMT), and generation and maintenance of cancer stem cells. In the wild-type state, HGF-MET signaling is essential for regeneration in liver and skin, and can control the EMT during development (1).

Combination MET- and EGFR-directed therapy in MET-overexpressing non-small cell lung cancers: time to move on to better biomarkers?