长链非编码RNA MEG3在人胶质瘤细胞中的表达及作用研究

目的 探究LncRNA MEG3对人胶质瘤细胞活力和凋亡的影响及其作用机制。方法 RT-qPCR检测人胶质瘤细胞系(U87)和正常星形胶质细胞系(NHAs)中MEG3、microRNA-21(miR-21)的表达;U87细胞单独转染MEG3质粒或同时转染MEG3质粒与miR-21 mimic后采用CCK-8检测细胞活力、TUNEL检测细胞凋亡、Western blot检测细胞内Bcl-2/Bax和Cleaved caspase-3表达。结果 与NHAs细胞相比,U87细胞中的MEG3表达明显下降,且miR-21表达明显上升。过表达MEG3明显降低U87的miR-21表达,抑制U87的活力,降低Bcl-2/Bax的水平,提高Cleaved caspase-3的含量,促进凋亡;共过表达MEG3和miR-21可明显增加U87的活力,提高Bcl-2/Bax的水平,降低Cleaved caspase-3的含量,抑制凋亡。结论 过表达MEG3通过抑制miR-21降低胶质瘤细胞的活力并促进其凋亡。

The expression and role of LncRNA MEG3 in human glioma cells

Objective The aim of this study was to illuminate effects of LncRNA MEG3 on the viability and apoptosis of human glioma cells as well as the mechanisms involved.Methods The expressions of MEG3 and microRNA-21(miR-21) in normal human astrocytes cell line(NHAs)and human glioma cell line(U87)was detected by Real-Time quantitative polymerase chain reaction(RT-qPCR).U87 cells was transfected with MEG3 plasmid alone or transfected with both MEG3 plasmid and miR-21 mimic,cell viability was detected by CCK-8 assay,cell apoptosis was detected by TUNNEL,and the expression of Bcl-2/Bax and Cleaved caspase-3 in cells was detected by Western blot.Results Compared with NHAs,the expression of MEG3 in U87 was significantly decreased and the expression of miR-21 was significantly increased.Overexpression of MEG3 significantly decreased the expression of miR-21 in U87 cells,inhibited the viability of U87 cells,decreased the level of Bcl-2/Bax,increased the content of Cleaved-caspase-3 to promote apoptosis;Co-overexpression of MEG3 and miR-21 significantly increased the viability of U87 cells,elevated Bcl-2/Bax levels,and decreased the expression of Cleaved caspase-3 to inhibit apoptosis.Conclusion Overexpression of MEG3 reduces the viability and promotes apoptosis of glioma cells by inhibiting miR-21.