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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.

miR-663 promotes NPC cell proliferation by directly targeting CDKN2A