pemt2-cDNA转染抑制大鼠肝癌CBRH-7919细胞周期相关蛋白的表达  

Transfection of pemt-2-cDNA inhibits the expression of cell cycle related proteins in rat CBRH-7919 hepatoma cells

作　　者：刘翠平[1] 邹伟[1] 王亮[1] 崔肇春[2] 

机构地区：[1]辽宁师范大学生命科学院,大连116029 [2]大连医科大学

出　　处：《中华肝脏病杂志》2006年第5期350-352,共3页Chinese Journal of Hepatology

基　　金：国家自然科学基金资助(39670809)

摘　　要：目的探讨磷脂酰乙醇胺-N-甲基转移酶2(PEMT2)的转染抑制肝癌细胞增殖的分子机制。方法将带有完整pemt2-cDNA质粒转染人大鼠肝癌CBRH-7919细胞,筛选出稳定传代并高表达PEMT2的细胞株,用Western blot, 比较了细胞周期调控因子细胞周期蛋白D1／细胞周期蛋白依赖性激酶(CDK)4、细胞周期蛋白E／CDK2、phospho-Rb、 caspase3、c-jun以及小窝蛋白caveolin的表达变化。结果在PEMT2高表达细胞中CDK2、CDK4、phospho-Rb和c jun表达下调,caspase3表达上调。结论 PEMT2的高表达降低CDK2和CDK4的表达水平,同时下调原癌基因phospho- Rb和c-jun的表达,抑制肝癌细胞由G1期进入S期,从而抑制肝癌细胞增殖并诱发肝癌细胞的凋亡。Objective To unravel the molecular mechanism of proliferation inhibiton reduced by transtection of pemt2- eDNA into rat CBRH-7919 hepatoma cells. Methods We started with the highly expressed PEMT2 clone. Cell culture and Western blotting techniques were used to examine the expression of cyclinD1/CDK4, cyclinFJCDK2, phospho-Rb, caspasc-3, c-jun and caveolins. Results Our results showed that CDK4, CDK2, phospho-Rb and c-jun were down regulated in the pcmt2 highly expressed cell clone. The high expression clone of pcmt2-transfected cells also showed over expression of caspase-3. Conclusion The reductions of proliferation and apoptosis of pcmt2 transfected cells could be related to the G 1 phase arrest induced by down-regulation of the cell cycle-associated proteins.

关 键 词：癌 肝细胞 细胞周期蛋白D1 磷脂酰乙醇胺-N-甲基转移酶2 细胞凋亡 

分 类 号：R735.7[医药卫生—肿瘤] R739.86[医药卫生—临床医学]