lncRNA MEG3通过下调miR-7-5p表达对鼻咽癌细胞放射敏感性的影响

目的 探讨lncRNA MEG3对鼻咽癌细胞的放射敏感性影响及潜在作用机制。方法 实验设置过表达对照组、过表达MEG3组、抑制miR-NC组、抑制miR-7-5p组、过表达对照+4 Gy组、过表达MEG3+4 Gy组、抑制miR-NC+4 Gy组、抑制miR-7-5p+4 Gy组、过表达MEG3+过表达miR-NC组、过表达MEG3+过表达miR-7-5p组。采用qRT-PCR检测miR-7-5p和MEG3表达;细胞克隆形成实验检测鼻咽癌细胞放射敏感性;流式细胞术检测细胞凋亡;双荧光素酶报告基因检测实验检测荧光活性。结果 MEG3在鼻咽癌组织和细胞系中低表达;过表达MEG3和抑制miR-7-5p表达可增加鼻咽癌细胞放射敏感性且促进细胞凋亡。MEG3可靶向调节miR-7-5p表达;过表达miR-7-5p逆转了过表达MEG3对鼻咽癌细胞放射增敏和促进细胞凋亡的作用。结论 过表达MEG3增加鼻咽癌细胞放射敏感性,并促进细胞凋亡,其机制可能与下调miR-7-5p有关。

Effect of lncRNA MEG3 on radiosensitivity of nasopharyngeal carcinoma cells by down-regulating miR-7-5p expression

Objective To investigate the effect and underlying mechanism of lncRNA MEG3 on the radiosensitivity of nasopharyngeal carcinoma cells.Methods this experiment, overexpression control group,MEG3 overexpression group,miR-NC inhibition group,miR-7-5p inhibition group,overexpression control+4 Gy group, MEG3 overexpression+4 Gygroup,miR-NC inhibition+4 Gy group, miR-7-5p inhibition+4 Gy group, MEG3 overexpression+miR-NC overexpression group,MEG3 overexpression+ miR-7-5p overexpression group were established. The expression of miR-7-5p and MEG3 was detected by qRT-PCR. The radiosensitivity of nasopharyngeal carcinoma cells was measured by clone formation assay. Cell apoptosis was assessed by flow cytometry. The fluorescence activity was evaluated by dual luciferase reporter assay.Results MEG3 was lowly expressed in nasopharyngeal carcinoma tissues and cells. Overexpression of MEG3 and inhibition of miR-7-5p expression increased the radiosensitivity of nasopharyngeal carcinoma cells and promoted radiation-induced cell apoptosis. MEG3 could targetedly regulate the miR-7-5p expression. Overexpression of miR-7-5p reversed the effect of overexpression of MEG3 on the sensitization of nasopharyngeal carcinoma cells and the promotion of apoptosis induced by radiation exposure.Conclusions Overexpression of MEG3 increases the radiosensitivity of nasopharyngeal carcinoma cells and promotes radiation-induced cell apoptosis. The mechanism may be related to the down-regulation of miR-7-5p expression.