ROS and Oxidative Stress Are Elevated in Mitosis during Asynchronous Cell Cycle Progression and Are Exacerbated by Mitotic Arrest
Name
nihms-1519775.pdf
Description
Accepted version
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673.73 KB
Format
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Checksum (MD5)
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Author(s)
Patterson, Jesse C
Joughin, Brian Alan
Van De Kooij, Lambertus W.
Lim, Daniel Cham-Chin
Yaffe, Michael B
Lauffenburger, Douglas A
Date Issued
February 2019
Journal
Cell systems
Publisher
Elsevier BV
Citation
Patterson, Jesse C. et al. “ROS and Oxidative Stress Are Elevated in Mitosis during Asynchronous Cell Cycle Progression and Are Exacerbated by Mitotic Arrest.” Cell systems (2019): 163-167.e2 © 2019 The Author(s)
Version
Author's final manuscript
Abstract
Although elevated levels of reactive oxygen species (ROS) have been observed in cancer cells and cancer cells aberrantly proliferate, it is not known whether the level of reactive oxygen species and the accumulation of oxidative damage to macromolecules vary across the cell cycle. Here, we measure the prevalence of reactive oxygen species and of biomolecule oxidation across the cell cycle in freely cycling cancer cells. We report that reactive oxygen species vary during the cell cycle and peak in mitosis, resulting in mitotic accumulation of oxidized protein cysteine residues. Prolonged mitotic arrest further increased the levels of ROS and the abundance of oxidatively damaged biomolecules, including cysteine-sulfenic-acid-containing proteins and 8-oxoguanine. These finding suggest that mitotic arrest agents may enhance the effects of ROS-dependent anticancer therapies. We studied connections between ROS and the cell cycle in unsynchronized cancer cells and using multiple independent assays found that ROS and oxidative damage to biomolecules are highest in mitosis and can be further enhanced by mitotic arrest.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Massachusetts Institute of Technology. Department of Biological Engineering
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/J.CELS.2019.01.005
