Silencing of c-Met by RNA interference inhibits the survival, proliferation, and invasion of nasopharyngeal carcinoma cells
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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.
Keywordsc-Met Nasopharyngeal carcinoma Proliferation Invasion Apoptosis
This study was supported by grants from the National Natural Science Foundation of China (no. 30801282), and the Research Fund for the Doctoral Program of Higher Education of China (no. 20020487062).
Conflicts of interest
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