PEMT2过表达抑制大鼠肝癌细胞PI3K,Akt的表达  

Overexpression of PEMT2 Inhibits PI3K and Akt Expression in Rat CBRH-7919 Hepatoma Cells

作　　者：李亚丽[1] 邹伟[2] 马克里[1] 夏泉[1] 崔肇春[1] 

机构地区：[1]大连医科大学生物化学与分子生物学教研室,大连116027 [2]辽宁师范大学生命科学学院,大连116029

出　　处：《生物化学与生物物理进展》2004年第4期345-349,共5页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金资助项目 ( 3 9670 80 9)~~

摘　　要：为探讨磷脂酰乙醇胺 N 甲基转移酶 2 (PEMT2 )过表达抑制大鼠肝癌细胞增殖的机制 ,构建了PEMT2高表达细胞克隆 ,并采用半定量RT PCR、免疫细胞化学及流式细胞仪技术 ,研究了PEMT2过表达对PI3K/Akt信号转导途径的影响 .实验结果显示 ,PEMT2过表达可抑制细胞PI3K和Akt的表达 ,并诱导细胞凋亡 .这一结果提示 ,PI3K/Akt信号转导途径下调可能是PEMT2抑制肝癌细胞增殖的部分机制 .In order to unravel the mechanism of inhibition of the cell proliferation induced by overexpression of PEMT2, the cell clone transfected with pemt2-cDNA was constructed and the effect of overexpression of PEMT2 on PI3K/Akt signaling pathway was investigated by the methods of RT-PCR, immunocytochemical and flow cytometry. The results show that the overexpression of PEMT2 could inhibit the expression of PI3K and Akt, and induce cell apoptosis. The results indicate that the down-regulating of PI3K/Akt signaling pathway could, at least partly, account for the inhibition of hepatoma cell proliferation induced by overexpression of PEMT2.

关 键 词：磷脂酰乙醇胺-N-甲基转移酶2 PEMT2 磷脂酰肌醇-3-激酶 大鼠 肝癌细胞 AKT 蛋白激酶B 凋亡 

分 类 号：R735.7[医药卫生—肿瘤] Q55[医药卫生—临床医学]