敲低STAT3基因可下调存活蛋白(survivin)水平促进U87MG胶质瘤细胞凋亡

Knockdown of STAT3 reduces the level of survivin and promotes the apoptosis of U87MG glioma cells

目的探讨信号转导子与转录激活子3(STAT3)特异性小干扰RNA(siRNA)对U87MG胶质瘤细胞的促凋亡作用及其作用机制。方法体外培养U87MG胶质瘤细胞,利用MTT法观察si STAT3质粒对细胞增殖的影响,通过流式细胞术及吖啶橙染色观察其对细胞凋亡影响,反转录PCR和Western blot法检测下调STAT3对存活蛋白(survivin)的调控效应。结果 si STAT3质粒可明显抑制U87MG胶质瘤细胞增殖,敲低STAT3可明显促进胶质瘤细胞凋亡,下调STAT3水平可明显降低survivin mRNA和蛋白水平。结论敲低U87MG细胞STAT3可下调survivn水平、促进胶质瘤细胞凋亡。

Objective To investigate the effect of signal transducer and activator of transcription（ STAT3）-specific siRNA（ si STAT3） on the apoptosis of U87 MG human glioma cells and its mechanism. Methods U87 MG glioma cells were cultured in vitro. The effect of si STAT3 on U87 MG human glioma cells was evaluated by MTT assay to observe cell proliferation and by flow cytometry and acridine orange staining to observe cell apoptosis. Reverse transcription PCR and Western blotting were used to detect the expression of survivin. Results Compared with mock and si-scrambled groups,si STAT3 expression plasmid inhibited the proliferation of U87 MG cells obviously. Flow cytometry and acridine orange staining showed that si STAT3 plasmid significantly promoted glioma cell apoptosis. In addition,si STAT3 plasmid significantly inhibited the mRNA and protein levels of survivin. Conclusion Knockdown of STAT3 in U87 MG cells can downregulate the level of survivin and remarkably promote the apoptosis of glioma cells.