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

SUMMARY 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.