Nuclear thioredoxin-1 is required to suppress cisplatin-mediated apoptosis of MCF-7 cells
Nuclear thioredoxin-1 is required to suppress cisplatin-mediated apoptosis of MCF-7 cells
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DOI：
10.1016/j.bbrc.2007.07.033
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发表时间：
2007-09-21
影响因子：
3.1
通讯作者：
Chen, Zheng-Wang
中科院分区：
文献类型：
--
作者：
Chen, Xiao-Ping;Liu, Shou;Chen, Zheng-Wang
硫氧还蛋白-1 （Trx-1）升高的不同细胞系对顺铂杀伤细胞的敏感性降低或增加。近年来，多项研究发现Trx-1的亚细胞定位与其功能密切相关。在这项研究中，我们探讨了核Trx-1与顺铂介导的乳腺癌细胞MCF-7凋亡的关系。首先，我们发现在Trx-1 cDNA转染的MCF-7细胞中，较高的Trx-1总量而核Trx-1未发生变化，并不影响顺铂诱导的细胞凋亡。其次，在Trx-1总量不变的情况下，较高的核Trx-1水平可以保护顺铂诱导的细胞凋亡。第三，高核Trx-1参与顺铂耐药细胞的顺铂耐药。同时，我们发现p53 mRNA水平与细胞核Trx-1水平密切相关。综上所述，我们得出结论，核Trx-1可能通过上调抗凋亡基因p53来抵抗顺铂诱导的MCF-7细胞凋亡。(c) 2007年Elsevier Inc.出版
Different cell line with increased thioredoxin-1 (Trx-1) showed a decreased or increased sensitivity to cell killing by cisplatin. Recently, several studies found that the subcellular localization of Trx-1 is closely associated with its functions. In this study, we explored the association of the nuclear Trx-1 with the cisplatin-mediated apoptosis of breast cancer cells MCF-7. Firstly, we found that higher total Trx-1 accompanied by no change of nuclear Trx-1 can not influence apoptosis induced by cisplatin in MCF-7 cells transferred with Trx-1 cDNA. Secondly, higher nuclear Trx-1 accompanied by no change of total Trx-1 can protect cells from apoptosis induced by cisplatin. Thirdly, high nuclear Trx-1 involves in the cisplatin-resistance in cisplatin-resistive cells. Meanwhile, we found that the mRNA level of p53 is closely correlated with the level of nuclear Trx-1. In summary, we concluded that the nuclear Trx-1 is required to resist apoptosis of MCF-7 cells induced by cisplatin, probably through up-regulating the anti-apoptotic gene, p53. (c) 2007 Published by Elsevier Inc.