Advances in the diagnosis and treatment of MET-variant digestive tract tumors

Figure 6 The c-MET pathway relays downstream signals to activate multiple oncogenic events to promote cell proliferation, migration, protein synthesis, and antiapoptosis. The c-MET pathway transmits downstream signals by activating its receptor tyrosine kinase, triggering multiple carcinogenic events. This pathway activates signaling pathways such as RAS/mitogen-activated protein kinase, phosphoinositide 3-kinase/protein kinase B, and promotes cell proliferation, migration, protein synthesis, and anti-apoptosis. HGF: Hepatocyte growth factor; MEK: Mitogen-activated protein/extracellular signal-regulated kinase; ERK: Extracellular signal-regulated kinase; RAC: Ras-related C3 botulinum toxin substrate; JNK: Jun N-terminal kinase; BAD: Bcl-2-associated death promoter; mTOR: Mechanistic target of rapamycin; Grb2: Growth factor receptor-bound protein 2; Gab1: Grb2-associated binder 1; STAT3: Signal transducer and activator of transcription 3; MDM2: Mouse double minute 2; PI3K: Phosphoinositide 3-kinase; AKT: Protein kinase B; NF-κB: Nuclear factor kappa B; EGCG: Epigallocatechin gallate.