Liu Cui-ping, Zou Wei, Wang Liang, Cui Zhao-chun
Department of Biology, Liaoning Normal University, Dalian 116029, China.
Zhonghua Gan Zang Bing Za Zhi. 2006 May;14(5):350-2.
To unravel the molecular mechanism of proliferation inhibition induced by transfection of pemt2-cDNA into rat CBRH-7919 hepatoma cells.
We started with the highly expressed PEMT2 clone. Cell culture and Western blotting techniques were used to examine the expression of cyclinD1/CDK4, cyclinE/CDK2, phospho-Rb, caspase-3, c-jun and caveolins.
Our results showed that CDK4, CDK2, phospho-Rb and c-jun were down regulated in the pemt2 highly expressed cell clone. The high expression clone of pemt2-transfected cells also showed over expression of caspase-3.
The reductions of proliferation and apoptosis of pemt2 transfected cells could be related to the G1 phase arrest induced by down-regulation of the cell cycle-associated proteins.
揭示将pemt2 - cDNA转染至大鼠CBRH - 7919肝癌细胞中所诱导的增殖抑制分子机制。
我们从高表达的PEMT2克隆开始。采用细胞培养和蛋白质免疫印迹技术检测细胞周期蛋白D1/细胞周期蛋白依赖性激酶4(cyclinD1/CDK4)、细胞周期蛋白E/细胞周期蛋白依赖性激酶2(cyclinE/CDK2)、磷酸化视网膜母细胞瘤蛋白(phospho - Rb)、半胱天冬酶 - 3(caspase - 3)、c - jun和小窝蛋白(caveolins)的表达。
我们的结果表明,在pemt2高表达细胞克隆中,CDK4、CDK2、磷酸化视网膜母细胞瘤蛋白和c - jun表达下调。pemt2转染细胞的高表达克隆还显示半胱天冬酶 - 3过表达。
pemt2转染细胞增殖和凋亡的减少可能与细胞周期相关蛋白下调诱导的G1期阻滞有关。