目的 探讨miR-21 过表达在替莫唑胺(TMZ)诱导胶质瘤U87 细胞增殖中的作用及其机制,明确miR-21 过表达在替莫唑胺临床治疗胶质瘤耐药中的作用.方法 Pre-miR-21 过表达载体转染U87 细胞,通过形态学观察,噻唑蓝(MTT)试验检测细胞增殖情况.Western 印迹验证Akt 和p-Akt 表达及检测PI3K 活性.结果 替莫唑胺可显著抑制U87 细胞生长,下调Akt 和p-Akt 表达及抑制PI3K 活性.U87 细胞预转染pre-miR-21 过表达载体后,替莫唑胺的这种效应可部分被miR-21 过表达所抑制.结论 miR-21 过表达可通过活化PI3K-AKT 通路部分抑制替莫唑胺诱导的U87 细胞凋亡,提示胶质瘤中miR-21 过表达可能是替莫唑胺临床治疗胶质瘤药物抵抗的一大新的因素.%Objective To explore the function and mechanism of miR-21 0verexpression in glioblastoma U87 cells proliferation inhibition induced by Temozolomide ( TMZ) . Methods PremiR-21 0ver-expression vectors were transfected into U87 cells. And the effects of cell proliferation were evaluated by morphological observation and MTT assay. The expressions of Akt and p-Akt were identified by Western blot , while PI3 K activity was detected. Results TMZ could effectively inhibit the growth of U87 cells , downregulate Akt and p-Akt expressions and inhibit PI3 K activity. After U87 cells were pre-transfected pre-miR-21 0ver-expression vectors, the effects induced by TMZ with partly inhibited by miR-21 0verexpression. Conclusions Over-express miR-21 may inhibit TMZ-induced apoptosis in U87 cells via PI3K-AKT pathway, which highlight the possibility of miR-21 overexpression in the clinical resistance to chemotherapeutic therapy of TMZ.
展开▼
