沉默lncRNA HOTAIR上调miR-17-5p表达增加U87R细胞放射敏感性

目的:探讨lncRNA HOTAIR对胶质瘤U87R细胞和移植瘤放射敏感性影响及潜在作用机制。方法:将阴性对照质粒、沉默HOTAIR质粒、过表达miR-NC质粒、过表达miR-17-5p质粒分别转染到U87R细胞中，记为沉默对照组、沉默HOTAIR组、过表达miR-NC组、过表达miR-17-5p组；以上各组细胞分别用...

Silencing lncRNA HOTAIR increases radiosensitivity of glioma cells by up-regulating miR-17-5p expression

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-NCsuppressing 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.