Nuclear thioredoxin-1 is required to suppress cisplatin-mediated apoptosis of MCF-7 cells

被引：28

作者：

Chen, Xiao-Ping ^{[1
]}

Liu, Shou ^{[1
]}

Tang, Wen-Xin ^{[1
]}

Chen, Zheng-Wang ^{[1
]}

机构：

[1] Huazhong Univ Technol, Coll Life Sci & Technol, Minist Educ, Key Lab Mol Biophys, Wuhan 430074, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 361卷 / 02期

基金：

中国国家自然科学基金;

关键词：

thioredoxin-1; p53; breast cancer; apoptosis; nucleus; NF-KAPPA-B; TRANSCRIPTION FACTOR; DIRECT ASSOCIATION; REDOX REGULATION; BREAST-CANCER; PATHWAY; EXPRESSION; RESISTANCE; PROTEIN-1; CARCINOMA;

D O I：

10.1016/j.bbrc.2007.07.033

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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.

引用

页码：362 / 366

页数：5

共 21 条

[1]

Thioredoxin is downstream of Smad7 in a pathway that promotes growth and suppresses cisplatin-induced apoptosis in pancreatic cancer [J].