Involvement of up-regulation of PUMA in non-steroidal anti-inflammatory drug-induced apoptosis

被引：39

作者：

Ishihara, Tomoaki ^{[1
]}

Hoshino, Tatsuya ^{[1
]}

Namba, Takushi ^{[1
]}

Tanaka, Ken-ichiro ^{[1
]}

Mizushima, Tohru ^{[1
]}

机构：

[1] Kumamoto Univ, Grad Sch Med & Pharmaceut Sci, Kumamoto 8620973, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 356卷 / 03期

基金：

日本科学技术振兴机构;

关键词：

PUMA; endoplasmic reticulum; ATF4; CHOP; apoptosis;

D O I：

10.1016/j.bbrc.2007.03.034

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：

NSAIDs such as celecoxib induce apoptosis in cancer cells. Although this apoptotic effect is involved in the anti-tumor activity associated with such drugs, the mechanism by which this occurs is not fully understood. We report here that various NSAIDs, including celecoxib, up-regulate PUMA, a Bcl-2 family protein with potent apoptosis-inducing activity, in human gastric carcinoma cell line, accompanying the induction of apoptosis. Experiments using siRNA and an intracellular Ca2+ chelator revealed that Ca2+-dependent up-regulation of ATF4 and CHOP is involved in this up-regulation of PUMA. The siRNA for PUMA inhibited the celecoxib-induced activation and translocation of Bax, release of cytochrome c into the cytosol and induction of apoptosis, suggesting that PUMA plays an important role in celecoxib-induced mitochondrial dysfunction and the resulting apoptosis. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：711 / 717

页数：7

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