中文摘要：

背景与目的：E2F3a是一种重要的转录激活因子，在多种肿瘤组织中均呈现表达上调。E2F3a在恶性化程度较高的神经胶质瘤中表达较高，目前它在胶质瘤细胞中的功能尚不清楚。本文的目的是研究E2F3。对U251胶质瘤细胞周期和凋亡的影响。方法：通过脂质体介导质粒转染在U251细胞中过表达E2F3a：用Western blotting检测细胞内E2F3a蛋白质的表达水平：用PT-核DNA染色结合流式细胞术分析细胞周期分布：用Annexin V—PE和7-AAD染色结合流式细胞术分析细胞凋亡比例；用实时荧光定量PCR方法测定细胞内A2、B1、D1和E细胞周期素mRNA的相对表达水平。结果：与空载体转染对照组相比．E2F3a过表达可将位于S期的细胞比例提高28％（P〈0．01），将位于G0/G1期和G2/M的细胞比例分别降低15％和13％（P〈0．01）。E2F3a过表达对细胞凋亡无明显影响。进一步研究发现，E2F3a可显著上调细胞周期素D1和E的mRNA表达．而不影响周期素A2和B1的mRNA表达。结论：E2F3a是胶质瘤细胞增殖的促进因子，它可通过上调细胞周期素D1和E的表达加速细胞由G，期进入S期。

英文摘要：

BACKGROUND ＆ OBJECTIVE： E2Fa is an important transcription activator and has been found to be upregulated in many tumor tissues. The expression level of E2F3a is higher in high-grade gliomas than that in lower-grade tumors, but the functional role of E2F3a has not been clarified. The objective of this article was to study the effects of E2F3a on cell cycle and apoptosis in U251 glioma cells. METHODS： Plasmid transfeetion mediated by liposome was employed to overexpress E2F3a in U251 cells. E2F3 protein expression was detected by Western blot. The nuclear DNA was stained with P1 and the distribution of cells in different cell cycle phase was analyzed by FACS. Annexin V-PE and 7-AAD staining coupled with FACS analysis was used to analyze the percentage of apoptotic cells. Relative expression levels of cyclin A2, B1, D1 and E mRNA were measured by real-time RT-PCR. RESULTS： As compared with control cells transfected with empty vector, E2F3a overexpression significantly increased the percentage of cells in S phase by 28% （P〈0.01） while decreased the percentage of cells in G0/G1 and GJM phases by 15% and 13% respectively. In contrast, E2F3a overexpression had no apparent effect on apoptosis. Further studies showed that E2F3a significantly upregulated the mRNA expression of cyclin D1 and cyclin E without affecting cyclin A2 and cyclin B1 level. CONCLUSION： Our results proved that E2F3a acts as a promoter of glioma proliferation, it promotes the G1/S transition through upregulation of cyclin D1 and cyclin E expression.