中文摘要：

目的 探讨Ras鸟苷酸结合蛋白超家族的新成员E（RhoE）过表达对人脑胶质瘤细胞株U251凋亡的影响及其机制.方法 应用脂质体介导的基因转染技术将Myc-N1、Myc-RhoE质粒分别转染人人脑胶质瘤U251细胞株,采用逆转录-聚合酶链反应（RT-PCR）与Western blot法测定对照组、N1-U251、RhoE-U251 3组细胞株中RhoE和细胞周期素（Cyclin） D1的mRNA与蛋白水平的变化,细胞计数试剂盒（CCK-8）法和流式细胞技术分析细胞的增殖与凋亡的变化.结果 RhoE-U251组中RhoE mRNA与蛋白表达水平较未转染组和转染空载体组明显升高,差异均有统计学意义（P＜0.05）.同时,RhoE-U251组中Cyclin Dl mRNA与蛋白表达水平较未转染组和转染空载体组明显降低,差异均有统计学意义（P＜0.05）.转染后胶质瘤细胞生长受到抑制,凋亡率也明显升高.结论 RhoE可能是一种抑癌基因,瞬时高表达可以抑制胶质瘤细胞株U251生长,其机制是通过下调细胞调控蛋白Cyclin D1促进细胞凋亡.

英文摘要：

Objective To investigate the effects of Ras homolog gene family,member E （RhoE）overexpression on the apoptosis of human glioma U251 cells and the mechanism.Methods The Myc-N1 and Myc-RhoE plasmids were transfected into human glioma U251 cells by Lipofectamine technology.The changes of RhoE and Cyclin D1 in transfected glioma cells were detected by reverse transcriptase-polymerase chain reaction （RT-PCR） and Western blotting.The cell proliferaion and apopotosis were analyzed by methyl thiazol tetrazolium （MTF） assay and flow cytometry.Results The RhoE mRNA and protein levels in RhoE-U251 group was significantly up-regulated compared to N1-U251 group and control group （P ＜0.05）,while the Cyclin D1 mRNA and protein levels in RhoE-U251 group were significantly suppressed.After overexpression of RhoE was up-regulated,the growth of these cells was inhibited and their apoptosis was obviously enhanced.Conclusion RhoE may be a tumor suppressor gene.Up-regulation of RhoE expression can down-regulate the Cyclin D1 expression,and then promote the apoptosis and inhibit the growth of human glioma U251 cells.