Reactive oxygen species regulate a balance between mitotic catastrophe and apoptosis

被引：9

作者：

Sorokina, Irina V. ^{[1
]}

Denisenko, Tatiana V. ^{[1
]}

Imreh, Gabriela ^{[2
]}

Gogvadze, Vladimir ^{[1
,2
]}

Zhivotovsky, Boris ^{[1
,2
]}

机构：

[1] Moscow MV Lomonosov State Univ, Fac Fundamental Med, Moscow 11999, Russia

[2] Karolinska Inst, Inst Environm Med, Div Toxicol, Box 210, S-17177 Stockholm, Sweden

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2016年 / 81卷

基金：

俄罗斯科学基金会; 瑞典研究理事会;

关键词：

Mitotic catastrophe; Apoptosis; Mitochondria; Reactive oxygen species; Tumor;

D O I：

10.1016/j.biocel.2016.11.006

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：

Mitotic catastrophe (MC) is a sequence of events resulting from premature or inappropriate entry of cells into mitosis that can be caused by chemical or physical stresses. There are several observations permitting to define MC as an oncosuppressive mechanism. MC can end up in apoptosis, necrosis or senescence. Here we show that the anticancer drug doxorubicin triggers DNA damage and MC independently of ROS production. In contrast, doxorubicin-induced apoptosis was found to be ROS-dependent. Antioxidants NAC or Trolox suppressed apoptosis, but facilitated MC development. Our data demonstrate that evasion of apoptosis and subsequent stimulation of MC can contribute to tumor cell elimination improving anticancer therapy. (C) 2016 Elsevier Ltd. All rights reserved.

引用

页码：133 / 136

页数：4

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