摘要
目的:研究CDK11p58基因对大鼠胰岛瘤细胞INS-1增殖及周期的影响.方法:INS-1细胞分为3组:实验组转染pcDNA3.0-CDK11p58质粒;空载体组转染pcDNA3.0空载体;空白对照组不加任何干扰48h后,Westernblot检测细胞中CDK11p58基因表达水平;MTT法检测转染CDK11p58基因对细胞增殖的影响;流式细胞仪检测转染CDK11p58基因后细胞周期的变化.结果:转染48h后,与空载体组相比,实验组CDK11p58基因的表达水平显著升高(P<0.01)INS-1细胞存活率下降(P<0.05),G1期细胞比例显著上升(69.87%±1.77%vs63.03%±2.66%P<0.01),细胞出现G1期阻滞.结论:CDK11p58基因与INS-1细胞增殖相关其高表达引起的细胞增殖速度放缓的作用机制可能与其所致的细胞G1期延长有关.
AIM： To observe the influences of CDK11p58 gene on the proliferation and cell cycle of rat insulinoma cell line INS-1. METHODS： Rat insulinoma INS-1 cells were divided into three groups： the experimental group transfected with plasmid pcDNA3.0-CDK11p58; empty vector group transfected with pcDNA3.0; blank control group without any interference. After 48 hours, the expression of CDK11p58 was detected by Western blot. The proliferation ac- tivities of the INS-1 cells ceils were assessed by the MTT assay. Cell cycle was analyzed by flow cytometry. RESULTS： In comparison with that in the empty vector group, the expression of CDK11p58 gene were significantly up-regulated in the experi- mental group after 48-h transfection （P 〈 0.01）. Over-expression of CDK11p58 gene suppressed the growth of INS-1 cells （P 〈 0.05）, and in- creased the Gl-phase cell proportion significantly （69.87% ± 1.77% vs 63.03% ± 2.66%, P 〈 0.01）. INS-1 cells were partly blocked at G1 phase. CONCLUSION： CDK11p58 gene is involved in the proliferation activity of INS-1 cells. Over-ex- pression of CDK11p58 gene may suppress INS-1 cell growth and the mechanisms may be due to the G1 phase arrest.
出处
《世界华人消化杂志》
CAS
北大核心
2009年第9期873-876,共4页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
No.30870989
国家973计划基金资助项目
No.2006CB503907
科技部专项基金资助项目
No.2004CCA01400
北京市自然科学基金资助项目
No.5062034~~
