SIRT4 regulates cancer cell survival and growth after stress

被引：51

作者：

Jeong, Seung Min ^{[1
,2
]}

Hwang, Sunsook ^{[3
,4
]}

Seong, Rho Hyun ^{[3
,4
]}

机构：

[1] Catholic Univ Korea, Coll Med, Dept Biochem, 222 Banpo Daero, Seoul 137701, South Korea

[2] Catholic Univ Korea, Coll Med, Inst Aging & Metab Dis, Seoul 137701, South Korea

[3] Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea

[4] Seoul Natl Univ, Inst Mol Biol & Genet, Seoul 151742, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2016年 / 470卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

SIRT4; Stress response; Cancer; Replicative stress; DNA-DAMAGE RESPONSE; GLUTAMINE-METABOLISM; SIRTUINS; TRANSFORMATION; INSTABILITY; PACLITAXEL; RESISTANCE; HALLMARK; RAS; MYC;

D O I：

10.1016/j.bbrc.2016.01.078

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：

Cellular stresses initiate well-coordinated signaling response pathways. As the proper regulation of stress is essential for cellular homeostasis, the defects of stress response pathways result in functional deficits and cell death. Although mitochondrial SIRT4 has been shown to be involved in cellular stress response and tumor suppression, its roles in survival and drug resistance of cancer cells are not well determined. Here we show that SIRT4 is a crucial regulator of the stress resistance of cancer cells. SIRT4 is highly induced by various cellular stresses and contributes to cell survival and growth after stresses. SIRT4 loss sensitizes cells to DNA damage or ER stress. Moreover, SIRT4 induction is required for tumorigenic transformation, as SIRT4 null cells are vulnerable to oncogene activation. Thus, these results suggest that SIRT4 has essential roles in stress resistance and may be an important therapeutic target for cancer treatment. (C) 2016 Elsevier Inc. All rights reserved.

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收藏

页码：251 / 256

页数：6

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