miR-206 enhances radiosensitivity of glioma cells by targeting MAPK1 pathway

Objective To investigate the signaling pathway probably targeted by miR-206 in regulation of the radiosensitivity of glioma cells, and to provide a basis for further understanding of its regulatory mechanism. Methods The miR-206 mimic or miR-206 inhibitor was transfected into U87 glioma cells. The activity of the MAPK pathway was inhibited by PD98059. The cells were exposed to radiation. MTT assay and colony formation assay were used to determine the changes in the radiosensitivity of cells. Quantitative RT-PCR and Western blot were used to determine the expression of miR-206 and MAPK1, respectively. TargetScan prediction and dual luciferase reporter system were used to verify the interaction between miR-206 and MAPK1. Results After exposure to radiation, the glioma cells had downregulated expression of miR-206 and upregulated expression of MAPK1. Overexpression of miR-206 induced by the miR-206 mimic reduced cell proliferation and colony formation ability and enhanced the radiosensitivity; inhibition of miR-206 expression by the miR-206 inhibitor reversed the effects of the miR-206 mimic. MAPK1 was predicted to be the possible target gene of miR-206 by TargetScan software. The dual luciferase reporter assay further confirmed the interaction between miR-206 and MAPK1. The expression of MAPK1 was negatively correlated with that of miR-206. The radiosensitivity of glioma cells was enhanced when the MAPK pathway was blocked by the inhibitor. Conclusions miR-206 probably targets MAPK1. It may regulate the radiosensitivity of glioma cells by inhibiting the activity of the MAPK signaling pathway. Key words: miR-206 gene; MAPK1 pathway; U87 cell line; Radiosensitivity