C-Met as a potential therapeutic target in triple negative breast cancer

Abstract

C-MET also known as hepatocyte growth factor receptor (HGFR) is a protein encoded by c-MET gene. It is a receptor tyrosine kinase which transfers signals from extracellular matrix to cytoplasm through binding with its single ligand HGF/SF-hepatocyte growth factor/scatter factor. C-Met signaling is required for many physiological processes including proliferation, scattering, morphogenesis, and survival. Awry c-Met signaling promotes breast cancer, and of aggressive phenotype. In all breast cancers, c-Met is overexpressed in 20%-30% of the cases and around 52% in triple negative breast cancer. Triple negative breast cancer (TNBC) is the most aggressive subgroup of breast cancers, specified as human epidermal growth factor receptor 2 (HER2) negative, estrogen receptor (ER) negative, and progesterone receptor (PR) negative. TNBC has high metastatic and mortality potential but lacks effective and selective therapeutic options. C-Met targeting drugs have potential role in targeting many cancers including TNBC, but to maximize the efficacy proper selection and study are required. We have discussed here about the c-MET signaling and biological signaling pathways and studies that suggest c-MET to be a novel target for targeted therapy for TNBC but which is yet to be investigated.