Objective To explore the expression level of microRNA-150-5p (miR-150-5p) in nasopharyngeal carcinoma tissue and its effects on proliferation of cancer cells and radiosensitivity.

Methods Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of miR-150-5p in nasopharyngeal carcinoma tissues and nasopharyngeal carcinoma cells. Nasopharyngeal carcinoma cells CNE2 were routinely cultured and transfected with miR-150-5p mimic, and were divided into control group (NC group) and miR-150-5p overexpression group (miR-150-5p mimic group). The proliferation ability of CNE2 cells in each group was detected by MTT assay; the apoptosis of CNE2 cells in each group was detected by flow cytometry; the Western blot was used to detect the expressions of phosphorylated phosphatidylinositol 3-kinase (pPI3K), phosphorylated protein kinase B (pAKT) and phosphorylated mammalian target of rapamycin (pmTOR) protein in cells in each group.

Results The expression level of miR-150-5p in nasopharyngeal carcinoma tissue was (0.74±0.39), which was significantly lower than (1.44±0.54) in paracancerous tissue (t=8.140, P < 0.001). After transfection with 48 hours, the expression level of miR-150-5p in CNE2 cells in the miR-150-5p mimic group was (6.31±1.20), which was significantly higher than (1.00±0.08)in the NC group (t=7.647, P < 0.001). The result of MTT experiment showed that the proliferation ability of CNE2 cells at 24, 48 and 72 hours in the miR-150-5p mimic group was significantly lower than that in the NC group (P < 0.05). After radiation with 0.5, 1.0, 2.0, 4.0, 8.0 and 16.0 Gy, the cell proliferation rates of the miR-150-5p mimic group were significantly lower than those of the NC group (P < 0.05). After radiation of CNE2 cells with 2 Gy, the apoptosis rate of cells in the miR-150-5p mimic group increased significantly when compared to that in the NC group, while the expression levels of pPI3K, pAKT and pmTOR protein in CNE2 cells decreased significantly when compared to that in the NC group (P < 0.05).

Conclusion The expression of miR-150-5p in nasopharyngeal carcinoma cells is down-regulated. Overexpression of miR-150-5p can inhibit the proliferation of nasopharyngeal carcinoma cells, promote cell apoptosis, and effectively enhance the radiosensitivity of nasopharyngeal carcinoma cells; its role may be played by regulating the PI3K/AKT/mTOR signal pathway, and miR-150-5p may be the target of drugs to enhance the radiosensitivity of nasopharyngeal carcinoma.