miR-663 promotes NPC cell proliferation by directly targeting CDKN2A.

MicroRNAs (miRs) act as important regulators during the development and progression of human cancer; however, the regulatory mechanism of miR-663 in nasopharyngeal carcinoma (NPC) remains unclear. The present study demonstrated that serum miR-663 levels were significantly increased in patients with NPC compared with healthy controls. In addition, the serum levels of miR-663 were associated with the grade, lymph node metastasis and clinical stage of NPC. The expression of miR-663 was increased in NPC C666-1 cells, compared with normal nasopharyngeal epithelial NP69 cells. The knockdown of miR-663 markedly decreased the proliferation of C666-1 cells through the induction of cell cycle arrest at the G1 stage. Cyclin-dependent kinase inhibitor 2A (CDKN2A) was hypothesized to be a putative target of miR-663. Further investigation confirmed that miR-663 was able to directly bind to the 3' untranslated region of CDKN2A mRNA, and to negatively regulate CDKN2A protein expression in C666-1 cells. Inhibition of CDKN2A expression attenuated the suppressive effects of miR-663 knockdown on the proliferation and cell cycle progression of C666-1 cells. In addition, it was observed that the mRNA and protein levels of CDKN2A were decreased in C666-1 cells compared with NP69 cells. In conclusion, the results of the present study demonstrated that miR-663 promoted the proliferation and cell cycle progression of NPC cells by directly targeting CDKN2A, suggesting that miR-663 may become a potential therapeutic target for the treatment of NPC.