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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
【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 .
【Abstract】 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.
【Key words】 phosphatidylethanolamine N-methyltransferase-2 (PEMT2); phosphatidylinostal-3-kinase (PI3K); protein kinase B(Akt); hepatoma; apoptosis;
- 【文献出处】 生物化学与生物物理进展 ,Progress In Biochemistry and Biophysics , 编辑部邮箱 ,2004年04期
- 【分类号】Q78
- 【被引频次】6
- 【下载频次】228