MicroRNA‑210 negatively regulates the radiosensitivity of nasopharyngeal carcinoma cells.

Abstract

Radiotherapy is one of the primary methods of treatment of malignant tumors, however, resistance to radiation is a major problem. The reasons for the radioresistance are still poorly understood. However, it is generally accepted that microRNAs (miRNAs or miRs) can regulate the radiosensitivity of tumors. The present study therefore aimed to identify specific miRNAs and their effects on radioresistant cells. More specifically, the aim was to investigate specific miRNAs and their effects on radioresistant tumor cells. The radioresistant tumor cells (CNE‑2R) were established using a dose gradient method, and the miRNA expression profiles of CNE‑2R cells and the parental cells (CNE‑2) were determined. The expression of miR‑210 in CNE‑2R cells was significantly higher than in CNE‑2 cells. CNE‑2R cells were transfected with LV‑hsa‑miR‑210‑inhibitor, and CNE‑2 cells were transfected with LV‑hsa‑miR‑210. The expression of miR‑210 was confirmed by reverse transcription quantitative‑polymerase chain reaction. The percentages of CNE‑2R‑miR‑210‑inhibitor and CNE‑2 cells in the G2/M phase were higher than in the CNE‑2R and CNE‑2‑miR‑210 cells, and the percentages of cells in S phase were lower than in the CNE‑2R and CNE‑2‑miR‑210 cells. Following 4Gy of radiation, CNE‑2R‑miR‑210‑inhibitor and CNE‑2 cells, which express low levels of miR‑210, had a higher apoptosis rate than CNE‑2R and CNE‑2‑miR‑210 cells. Following 4, 8 and 12Gy of radiation, cell viability and survival fraction of CNE‑2R‑miR‑210‑inhibitor cells were lower than those of CNE‑2R and CNE‑2‑miR‑210 cells, and similar to those of CNE‑2 cells. Together, these findings strongly suggest that miR‑210 negatively regulates the radiosensitivity of tumor cells, and may therefore have therapeutic potential for the treatment of radiation resistance.