MET is a receptor tyrosine kinase that serves as the high-affinity receptor for hepatocyte growth factor (HGF), a critical ligand for normal mammalian development 1. Upon HGF binding, MET activates downstream signaling cascades including MAPK, PI3K/Akt/mTOR, and STAT3 pathways to regulate cell proliferation, migration, morphogenic differentiation, and angiogenesis 2. MET is essential for normal developmental processes such as cell migration, three-dimensional tubular structure organization, liver development, and neuron differentiation. In cancer pathogenesis, MET becomes deregulated through ligand overexpression, receptor overexpression, gene amplification, and activating mutations 3. Aberrant MET signaling drives tumor initiation, proliferation, invasion, and metastasis across multiple cancer types including hepatocellular carcinoma, renal cell carcinoma, non-small cell lung cancer, gastric cancer, and glioblastoma 45. MET overexpression and amplification correlate with poor prognosis, advanced disease, lymph node metastasis, and therapeutic resistance 67. Cancer cells exploit MET's physiological functions to enable invasion and immune evasion within the tumor microenvironment 4. Given these oncogenic roles, MET inhibition has emerged as a validated therapeutic strategy, with multiple inhibitors entering clinical trials for cancer treatment 18.