Silencing of c-Met by RNA interference inhibits the survival, proliferation, and invasion of nasopharyngeal carcinoma cells.

c-Met is a tyrosine kinase receptor that mediates pleiotropic cellular responses following its activation by hepatocyte growth factor. The overexpression of c-Met in nasopharyngeal carcinoma (NPC) has been described recently, but the functional role of c-Met in NPC remains incompletely understood. This study aimed to investigate the potential mechanism by which c-Met contributes to the tumorigenesis of NPC. In the present study, by using RNA interference we silenced the expression of c-Met in CNE-2 cells, a poorly differentiated NPC cell line. Our in vitro studies showed that shRNA-mediated depletion of c-Met resulted in the suppression of proliferation, migration, and invasion, as well as an increase in the apoptosis of CNE-2 cells. Moreover, in xenograft nude mice we demonstrated that the depletion of c-Met resulted in reduced tumor growth and increased apoptosis in xenografts. Taken together, these results suggest that c-Met plays an oncogenic role in the development of NPC and reveal it as a potential novel therapeutic target for NPC.