同源重组修复基因RAD51可提高PTEN缺失细胞基因组稳定性  

Homologous recombination repair gene RAD51 could increase the genomic stability of PTEN deleted cells

作　　者：陈忠民[1,2] 徐勤枝[1] 胡迎春[1] 霍艳英[1] 周平坤[1] 吴德昌[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所,北京100850 [2]中国人民解放军第二炮兵防疫中心,北京100071

出　　处：《癌变．畸变．突变》2011年第6期406-409,共4页Carcinogenesis,Teratogenesis & Mutagenesis

基　　金：国家重大科学研究计划(2007CB914603);国家自然科学基金项目(30872136)

摘　　要：目的:研究同源重组修复基因RAD51对PTEN缺失小鼠胚胎成纤维细胞基因组稳定性的影响。方法:应用免疫荧光和中性单细胞电泳技术观察PTEN缺失后自发性和辐射诱导DNA双链断裂情况;并构建PTEN缺失细胞稳定转染RAD51的细胞系,γ射线照射后检测细胞存活率。结果:PTEN缺失导致细胞自发性和辐射诱导DNA双链断裂增多;转染RAD51后细胞存活率增高,辐射诱导的DNA双链断裂减少。结论:同源重组修复基因RAD51可以提高PTEN缺失细胞基因组稳定性。OBJECTIVE：To explore the effect of genomic stability of PTEN-deficient mice embryonic fibroblasts after transfection with RAD51,an important homologous recombination repair gene.METHODS： Immunofluorescence assay was used to observe the number of spontaneousγ-H2AX foci.Neutral single cell gel electrophoresis was applied to detect spontaneous and radiation-induced DNA double-strand breaks in both PTEN-deficient and PTEN wild-type cells.RESULTS：PTEN deletion led to an increase of spontaneousγ-H2AX foci and the length of tail moment,indicating DNA double-strand breaks.Transfection with RAD51 increased cell survival and decreased radiation-induced DNA double-strand breaks of PTEN-deficient cells.CONCLUSION：Homologous recombination gene RAD51 could increase genomic stability of PTEN-deficient cells.

关 键 词：PTEN RAD51 基因组稳定性 

分 类 号：Q75[生物学—分子生物学]