Role of the MET-HGF axis in colorectal cancer: precepts and prospects

Colorectal cancer (CRC) accounts for 10% of all cancer-related mortality globally. Despite significant therapeutic advances, overall survival is limited. The restricted repertoire of therapies necessitates investigation into novel pathways of colorectal carcinogenesis. The proto-oncogene MET encodes a receptor tyrosine kinase that acts as a receptor for the HGF. Dysregulation of this MET-HGF axis has been implicated in proliferation, survival and metastasis in various tumor types including CRC. Increased MET-HGF expression correlates with tumor progression and adverse survival outcome. The prognostic impact argues in favor of employing inhibition of the MET-HGF axis as a promising new therapeutic strategy. Future investigations should endeavor to assess the potential application of targeted MET-HGF therapy in CRC and towards patient selection.