TAK1 kinase determines TRAIL sensitivity by modulating reactive oxygen species and cIAP

被引：33

作者：

Morioka, S. ^{[1
,2
]}

Omori, E. ^{[1
]}

Kajino, T. ^{[2
]}

Kajino-Sakamoto, R. ^{[1
]}

Matsumoto, K. ^{[2
,3
]}

Ninomiya-Tsuji, J. ^{[1
]}

机构：

[1] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA

[2] Nagoya Univ, Grad Sch Sci, Dept Mol Biol, Nagoya, Aichi 4648601, Japan

[3] Japan Sci & Technol Agcy, SORST, Tokyo, Japan

来源：

ONCOGENE | 2009年 / 28卷 / 23期

关键词：

TAK1; TRAIL; reactive oxygen species; cIAP; apoptosis; NF-KAPPA-B; APOPTOSIS-INDUCING LIGAND; HUMAN CANCER-CELLS; INDUCED DEATH; CASPASE-8; ACTIVATION; SIGNALING PATHWAYS; DECOY RECEPTORS; TARGETING DEATH; JNK ACTIVATION; UP-REGULATION;

D O I：

10.1038/onc.2009.110

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：

TNF-related apoptosis-inducing ligand (TRAIL) is a potent inducer of cell death in several cancer cells, but many cells are resistant to TRAIL. The mechanism that determines sensitivity to TRAIL-killing is still elusive. Here we report that deletion of TAK1 kinase greatly increased activation of caspase-3 and cell death after TRAIL stimulation in keratinocytes, fibroblasts and cancer cells. Although TAK1 kinase is involved in NF-kappa B pathway, ablation of NF-kappa B did not alter sensitivity to TRAIL. We found that TRAIL could induce accumulation of reactive oxygen species (ROS) when TAK1 was deleted. Furthermore, we found that TAK1 deletion induced TRAIL-dependent downregulation of cIAP, which enhanced activation of caspase-3. These results show that TAK1 deletion facilitates TRAIL-induced cell death by activating caspase through ROS and downregulation of cIAP. Thus, inhibition of TAK1 can be an effective approach to increase TRAIL sensitivity. Oncogene (2009) 28, 2257-2265; doi: 10.1038/onc.2009.110; published online 4 May 2009

引用

页码：2257 / 2265

页数：9

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