Reactive oxygen species regulate a balance between mitotic catastrophe and apoptosis

Irina V Sorokina; Tatiana V Denisenko; Gabriela Imreh; Vladimir Gogvadze; Boris Zhivotovsky

doi:10.1016/j.biocel.2016.11.006

Reactive oxygen species regulate a balance between mitotic catastrophe and apoptosis

Int J Biochem Cell Biol. 2016 Dec;81(Pt A):133-136. doi: 10.1016/j.biocel.2016.11.006. Epub 2016 Nov 11.

Authors

Irina V Sorokina¹, Tatiana V Denisenko¹, Gabriela Imreh², Vladimir Gogvadze³, Boris Zhivotovsky⁴

Affiliations

¹ Faculty of Fundamental Medicine, MV Lomonosov Moscow State University, 11999 Moscow, Russia.
² Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 17177 Stockholm, Sweden.
³ Faculty of Fundamental Medicine, MV Lomonosov Moscow State University, 11999 Moscow, Russia; Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 17177 Stockholm, Sweden.
⁴ Faculty of Fundamental Medicine, MV Lomonosov Moscow State University, 11999 Moscow, Russia; Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 17177 Stockholm, Sweden. Electronic address: Boris.Zhivotovsky@ki.se.

PMID: 27840153
DOI: 10.1016/j.biocel.2016.11.006

Abstract

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.

Keywords: Apoptosis; Mitochondria; Mitotic catastrophe; Reactive oxygen species; Tumor.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Apoptosis* / drug effects
Doxorubicin / pharmacology
HCT116 Cells
Humans
Mitochondria / drug effects
Mitochondria / metabolism
Mitosis* / drug effects
Reactive Oxygen Species / metabolism*

Substances

Reactive Oxygen Species
Doxorubicin