摘要
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.
出处
《中华医学遗传学杂志》
CAS
CSCD
北大核心
2008年第5期497-501,共5页
Chinese Journal of Medical Genetics
基金
国家自然科学基金(30672165)
江苏省医学重点人才项目(RC2007061)