Down‐regulation of adenine nucleotide translocase 3 and its role in camptothecin‐induced apoptosis in human hepatoma QGY7703 cells
Down‐regulation of adenine nucleotide translocase 3 and its role in camptothecin‐induced apoptosis in human hepatoma QGY7703 cells
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DOI：
10.1016/j.febslet.2008.12.029
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发表时间：
2009-01
期刊：
影响因子：
3.5
通讯作者：
Zhen-lin Hu;Xueqing Guo;Qi Yu;Lei Qiu;Jianzhong Li;K. Ying;Cheng Guo;Jun-ping Zhang
中科院分区：
文献类型：
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作者：
Zhen-lin Hu;Xueqing Guo;Qi Yu;Lei Qiu;Jianzhong Li;K. Ying;Cheng Guo;Jun-ping Zhang
腺嘌呤核苷酸转位酶（ANT）是线粒体通透性转换孔（MPTP）的核心成分，在细胞死亡中起关键作用。然而，其在喜树碱（CPT）诱导的细胞凋亡中的作用尚未得到研究。我们发现CPT诱导QGY7703细胞凋亡并下调ANT3的表达。使用ANT3敲除和过表达实验，我们提供了进一步的证据表明，ANT3通过诱导MPTP在CPT诱导的细胞凋亡中起着贡献作用。我们推测CPT刺激后ANT 3的下调可能是CPT获得性耐药机制的分子基础的一部分。
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.