ABSTRACT
Objective:To investigate the effect of lncRNA HOTAIR on the radiosensitivity of glioma cells and its underlying mechanism.Methods:The negative control plasmid, HOTAIR silencing plasmid, miR-NC over expressing plasmid, miR-17-5p over expressing plasmid were transfected into U87R cells, and assigned intothe silencing control, HOTAIR silencing, miR-NC over expressing and miR-17-5 pover expressing groups. Cells in the the above groups were irradiated at a dose of 4Gy, and recorded as silencing control+ 4Gy group, HOTAIRsilencing+ 4Gy group, miR-NC over expressing+ 4Gy group and miR-17-5p over expressing+ 4Gy group. The HOTAIR silencing plasmid, miR-NC suppressing plasmid and miR-17-5p suppressing plasmid were co-transfected into U87R cells and recorded as the HOTAIR silencing+ miR-NC suppressing group and HOTAIR silencing+ miR-17-5p suppressing group. All procedures were transfected by the liposome method. The expression of miR-17-5p and HOTAIR was detected by qRT-PCR. The radio sensitivity of glioma cells was evaluated by cell clone formation assay. The cell apoptosis was assessed by flow cytometry. The fluorescence activity was assessed by dual luciferase reporter assay.Results:HOTAIR was highly expressed in the radiation-resistant glioma cells. Silencing HOTAIR and over-expressing miR-17-5p could increase the radiosensitivity of U87R cells and promote radiation-induced apoptosis of U87R cells. HOTAIR could target and regulate the miR-17-5p expression. Suppressing miR-17-5p reversed the effect of silencing HOTAIR on U87R cell sensitization and promoting radiation-induced U87R cell apoptosis.Conclusions:Silencing lncRNA HOTAIR yields radiation sensitization and promotes radiation-induced apoptosis in glioma cells. The mechanism may be related to the regulation of miR-17-5p.