C-MET

Mesenchymal-epithelial transition factor (C-MET) is a transmembrane receptor with autophosphorylation activity encoded by the proto-oncogene MET. Its binding with hepatocyte growth factor (HGF) plays an important role in regulating cell proliferation, differentiation, migration, and apoptosis. C-MET is expressed in lung cancer, liver cancer, gastric cancer, colorectal cancer, kidney cancer, pancreatic cancer, breast cancer and other tumors, and its abnormal changes can be caused by MET gene mutation, amplification, fusion, or ligand dependent C-MET protein continuous activation. Moreover, C-MET expression level is positively correlated with the tumor malignancy, which may be because it will abnormally activate signaling pathways such as RAS/MAPK and P13K/AKT to promote proliferation and inhibit apoptosis of cancer cell after binding to HGF. Some research also suggested that C-MET may synergize with PD-1/PD-L1 pathway to mediate tumor immune escape. In addition, small molecule tyrosine kinase inhibitors and monoclonal antibodies targeting C-MET have become a research highlight in tumor treatment.