Fig. 1

Schematic representation of the HGF/MET signaling pathway [13]. The binding of HGF to MET induces conformational changes, receptor dimerization, trans-phosphorylation of tyrosine residues in the catalytic domain of MET, and phosphorylation of tyrosine residues in the carboxyl-terminal tail. The phosphorylated tyrosine residues create docking sites for several adaptor molecules and kinase substrates. MET activation results in subsequent activation of signaling pathways that include ERK/MAPK, PI3K/AKT and STAT3, which mediate MET-dependent cell proliferation, survival, migration, and invasion. Capmatinib, tepotinib, and savolitinib block the phosphorylation of tyrosine residues