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MicroRNA-222 (miR‑222) has been reported to be involved in the initiation, development and metastasis of tumors, as well as conferring resistance to chemotherapeutic drugs or radiotherapy in various types of cancer. However, the role and the underlying molecular mechanism of miR‑222 specifically in nasopharyngeal carcinoma (NPC) remains unclear. Thus, the biological function and underlying mechanism of in miR‑222 was investigated in NPC tissue specimens and cell lines. miR‑222 was upregulated in NPC tissues and malignant cell lines compared with adjacent normal samples and cell lines. miR‑222 upregulation significantly increased NPC cell proliferation, colony formation and cell apoptosis. Furthermore, miR‑222 upregulation conferred radioresistance. It was also confirmed that phosphatase and tensin homolog (PTEN) was a direct target for miR‑222 in NPC cells. Alteration of miR‑222 expression was demonstrated to regulate the phosphoinositide 3‑kinase/protein kinase B pathway in NPC cells. These results suggest that miR‑222 may act as an oncomir in NPC by targeting PTEN, and has potential as a therapeutic target in NPC.

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN