| PEMT2过表达抑制大鼠肝癌细胞PI3K, Akt的表达(英) |
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| 引用本文： | 李亚丽,邹伟,马克里,夏泉,崔肇春. PEMT2过表达抑制大鼠肝癌细胞PI3K, Akt的表达(英)[J]. 生物化学与生物物理进展, 2004, 31(4): 345-349 |
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| 作者姓名： | 李亚丽 邹伟 马克里 夏泉 崔肇春 |
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| 作者单位： | 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 |
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| 基金项目： | 国家自然科学基金资助项目（39670809）. |
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| 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.
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| 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（PI3K），蛋白激酶B(Akt)，肝癌，凋亡 |
| 收稿时间： | 2003-09-17 |
| 修稿时间： | 2003-11-10 |
Overexpression of PEMT2 Inhibits PI3K and Akt Expression in Rat CBRH-7919 Hepatoma Cells |
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| LI Ya-Li,ZOU Wei,MA Ke-Li,XIA Quan and CUI Zhao-Chun. Overexpression of PEMT2 Inhibits PI3K and Akt Expression in Rat CBRH-7919 Hepatoma Cells[J]. Progress In Biochemistry and Biophysics, 2004, 31(4): 345-349 |
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| Authors: | LI Ya-Li ZOU Wei MA Ke-Li XIA Quan CUI Zhao-Chun |
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| Affiliation: | Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian 116027, China;Department of Biology, Liaoning Normal University, Dalian 116029, China;Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian 116027, China;Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian 116027, China;Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian 116027, China |
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| 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. |
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| Keywords: | phosphatidylethanolamine N-methyltransferase-2 (PEMT2) phosphatidylinostal-3-kinase (PI3K) protein kinase B(Akt) hepatoma apoptosis |
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