Down-regulation of adenine nucleotide translocase 3 and its role in camptothecin-induced apoptosis in human hepatoma QGY7703 cells

被引：13

作者：

Hu, Zhenlin ^{[1
]}

Guo, Xueqing ^{[2
]}

Yu, Qi ^{[3
]}

Qiu, Lei ^{[1
]}

Li, Jianzhong ^{[1
]}

Ying, Kang ^{[2
]}

Guo, Cheng ^{[3
]}

Zhang, Junping ^{[1
]}

机构：

[1] Second Mil Med Univ, Sch Pharm, Dept Biochem Pharm, Shanghai 200433, Peoples R China

[2] Fudan Univ, Sch Life Sci, Inst Genet, State Key Lab Genet Engn, Shanghai 200433, Peoples R China

[3] Shanghai Jiao Tong Univ, Affiliated People Hosp 6, Dept Pharm, Shanghai 200233, Peoples R China

来源：

FEBS LETTERS | 2009年 / 583卷 / 02期

关键词：

Camptothecin; Adenine nucleotide translocase 3; Apoptosis; Hepatoma QGY7703 cell; Mitochondrial permeability transition pore; PERMEABILITY TRANSITION PORE; MITOCHONDRIAL CONTROL; GENE-EXPRESSION; DNA-DAMAGE; BAX; DEATH; MICROARRAY; COMPONENT; BCL-2; MYC;

D O I：

10.1016/j.febslet.2008.12.029

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Adenine nucleotide translocase (ANT) is known as a core component of the mitochondrial permeability transition pore (MPTP) and a key player in cell death. However, its role in camptothecin (CPT)-induced apoptosis has not been examined. We showed that CPT-induced apoptosis in QGY7703 cells and down-regulated the expression of ANT3. Using ANT3 knock-out and overexpression experiments, we provide further evidence that ANT3 plays a contributive role in CPT-induced apoptosis through induction of MPTP. We speculate that the down-regulation of ANT3 upon stimulation with CPT may be part of the molecular basis underlying the mechanism of acquired resistance to CPT. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：383 / 388

页数：6

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