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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.
Objective: To study the effect of CDK11p58 gene on the proliferation and cell cycle of INS-1 cells in rat.Methods: The INS-1 cells were divided into 3 groups: pcDNA3.0-CDK11p58 plasmid was transfected into the experiment group, and pcDNA3.0 The expression of CDK11p58 was detected by Western blotting. The effect of CDK11p58 transfection on cell proliferation was detected by MTT assay. The cell cycle was analyzed by flow cytometry after CDK11p58 transfection. Results: Compared with the control group, the expression of CDK11p58 gene was significantly increased (P <0.01), the survival rate of INS-1 cells decreased significantly (P <0.05), and the percentage of cells in G1 phase increased significantly % ± 1.77% vs63.03% ± 2.66% P <0.01) .Conclusion: The mechanism of the slowdown of cell proliferation induced by the high expression of CDK11p58 gene and INS-1cells may be related to Proliferation of cells caused by G1 phase.