CAJ | 학술논문

目的探讨miR -21过表达在替莫唑胺诱导胶质瘤U87细胞凋亡中的作用及其机制.方法 miR - 21过表达载体转染U87细胞,Hoechst 33258染色和流式细胞分析凋亡,Westem blot验证Bax和Bcl -2表达及检测Caspase -3活性.结果替莫唑胺可显著诱导U87细胞凋亡,上调Bax 表达、下调Bcl-2表达及增加Caspase -3活性.U87细胞预转染miR -21过表达载体后,替莫唑胺的这种效应可部分被抑制.结论 miR -21过表达可通过下调Bax/Bcl -2比率及Caspase -3活性部分抑制替莫唑胺诱导的U87细胞凋亡,提示胶质瘤中miR -21过表达可能是胶质瘤对替莫唑胺耐药的一大新的因素.
목적 탐토miR -21과표체재체막서알유도효질류U87세포조망중적작용급기궤제.방법 miR - 21과표체재체전염U87세포,Hoechst 33258염색화류식세포분석조망,Westem blot험증Bax화Bcl -2표체급검측Caspase -3활성.결과 체막서알가현저유도U87세포조망,상조Bax 표체、하조Bcl-2표체급증가Caspase -3활성.U87세포예전염miR -21과표체재체후,체막서알적저충효응가부분피억제.결론 miR -21과표체가통과하조Bax/Bcl -2비솔급Caspase -3활성부분억제체막서알유도적U87세포조망,제시효질류중miR -21과표체가능시효질류대체막서알내약적일대신적인소.
Objective To explore the function and mechanism of miR - 21 overexpression in glioblastoma U87 cells apoptosis induced by temozolomide (TMZ).Methods miR- 21 over- expression vectors were transfected into U87 cells.After that,cell apoptosis was analyzed by Hoechst 33258 staining and flow cytometry.And the expression of Bax and Bcl - 2 was identified by Western blot,while Caspase - 3 activity was detected.Results TMZ could effectively induce the apoptosis of U87 ceils,upregulate the Bax expression,downregulate the Bcl -2 expression and increase PI3K activity.However,after U87 cells were pre -transfected with miR- 21 over- expression vectors, the effects induced by TMZ was partly inhibited.Conclusion Over- expression miR- 21 could inhibit TMZ -induced apoptosis in U87 cells,at least in part,by decreasing Bax/Bcl- 2 ratio and Caspase- 3 activity,which highlighted the possibility of miR- 21 overexpression in resistance to chemotherapy TMZ in glioblastomas.