探讨人胶质瘤细胞系U87细胞中反义miR-21诱导凋亡机制

The mechanism of apoptosis in human U87 glioma cells induced by miR-21 antisense oligonucleotide

目的探讨下调miR-21诱导人胶质瘤细胞系U87细胞凋亡机制。方法应用化学方法合成的反义miR-21寡聚核苷酸（anti—miR-21），通过瞬转法转染U87细胞，检测U87细胞凋亡、增殖、侵袭等变化，并结合生物信息学分析、Western印迹验证在U87细胞中miR-21和PTEN基因及caspase间关系。结果体外转染反义miR-21寡聚核苷酸能明显抑制U87细胞生长，诱导其凋亡，降低侵袭能力；增加caspase-3表达活性，活化caspase-9表达，但不影响VIEN和caspase-8表达。结论miR-21可能是人胶质瘤U87细胞的抗凋亡微RNA（microRNA，miRNA），反义miR-21可能通过caspase-9、3而不是PTEN诱导肿瘤细胞凋亡。

Objective To investigate the mechanism of U87 cell apoptosis induced by inhibiting miR-21 expression. Methods Antisense oligonucleotides of miR-21 were chemically synthesized and transfected into U87 cells. The apoptosis, proliferation, and invasion of the cells were evaluated. The relationship between miR-21 and PTEN or caspase was identified by bioinformatics and Westem blot. Results Inhibiting miR-21 expression led to U87 cell growth suppression,apoptosis induction, invasion reduction, caspase-3 activity elevation and caspase-9 activation, but did not affect FTEN and caspase-8 expression. Conclusion miR-21 may function as an antiapoptotic miRNA in U87 cells. Inhibiting miR-21 expression could induce U87 cell apoptosis via caspase-9 and 3 activation, but not PTEN activation.