Background: In the current study, we aim to demonstrate the biological function and molecular regulatory mechanisms of miR-221 in human nasopharyngeal carcinoma (NPC). Methods: The quantitative real time-polymerase chain reaction was used to measure the expression of miR-221 in NPC clinical tissues and cells. And the flow cytometry assay was used to demonstrate the role of miR-221 on cell cycle, and the potential target of miR-221 was predicted and identified using luciferase reporter assay.Results: Our results demonstrate that miR-221 expression was significantly decreased in NPC tissues and cell lines. We also confirmed that inhibition of miR-221 could induce G1/S cell cycle transition through upregulation of the cyclin D-CDK4/6 complex but not cyclin E-CDK2 complexes. Furthermore, luciferase reporter assay demonstrated that miR-221 could directly bind to the 3’-UTR of FBXW11. FBXW11 expression was found to increase in NPC, and was inversely correlated with miR-221 expression; thus, FBXW11 expression interfered in the biological function of miR-221. We further confirmed that miR-221 targeted FBXW11 to inhibit proliferation and promote apoptosis in NPC cell lines through regulating the PTEN signaling pathway. Conclusion: our findings suggest that miR-221 plays an important role as a tumor suppressive factor in the occurrence and progression of NPC.
