E1A对转染了Ras的原代人皮肤成纤维细胞生长调控的研究  

Transfection with human adenovirus type 5 early-region 1A protects the primary human fibroblasts from ras-induced premature senescence in vitro

作　　者：李亦蕾[1] 郑萍[1] 许重远[1] 晏媛[1] 

机构地区：[1]南方医科大学南方医院药学部,广东广州510515

出　　处：《南方医科大学学报》2008年第10期1820-1823,共4页Journal of Southern Medical University

基　　金：广东省医学科学技术研究基金(B2006101)~~

摘　　要：目的癌基因ras的单独激活可导致细胞早期衰老,这被认为是一种抑制肿瘤形成的细胞防御机制,我们在人类成纤维细胞研究了病毒癌基因E1A对Ras激活的调控作用。方法在人成纤维细胞转染E1A、E1A1-143、或空载体(BP)和Ha-RasV12或其空载体(WH),确定其转染细胞的生长曲线和细胞凋亡比例。结果单独表达E1A或Ha-RasV12可显著抑制人成纤维细胞的生长,当E1A或E1A1-143与Ha-RasV12联合转染人成纤维细胞后,细胞增殖活跃。结论E1A可保护人类成纤维细胞免于Ras诱导的细胞早期衰老,其生物学活性位于E1A的氨基端。Objective To investigate the role of human adenovirus type 5 （Ad5） early-region 1A （E1A） in premature senescence of human fibroblasts induced by Ras activation. Methods Human fibroblasts were cotransduced with E1A, E 1A 1-143, or their vector （BP） and Ha-RasV 12 or its vector （WH）. The growth curves and percentages of the apoptotic cells were determined. Results Expression of E1A or Ha-RasV12 in human fibroblasts significantly inhibited the cell growth. Transduction of Ha-RasV12 along with E1A or E1A 1-143 into human fibroblast cells resulted in active and rapid cell proliferation. Conclusion E1A can rescue human fibroblasts from Ras-induced premature senescence, and the senescence bypassing activity of E1A resides in its NH2 terminus.

关 键 词：癌基因 E1A 人成纤维细胞 RAS 

分 类 号：Q78[生物学—分子生物学]