期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 103, 期 -, 页码 177-187出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2016.12.031
关键词
ROS; Mitotic arrest; Spindle; Aurora A; Phosphorylation
资金
- Ministry of Science and Technology of People's Republic of China [2016YFC1202401]
- National Natural Science Foundation of China [30871240, 31270798]
Oxidative stress contributes to the oxidative modification of cellular components, including lipids, proteins and DNA, and results in DNA damage, cell cycle arrest, cellular dysfunction and apoptosis. However, the mechanism underlying oxidative stress-induced mitotic abnormalities is not fully understood. In this study, we demonstrated that exogenous and endogenous reactive oxygen species (ROS) promoted mitotic arrest. Delayed formation and abnormal function of the mitotic spindle, which directly impeded mitosis and promoted abnormal chromosome separation, was responsible for ROS-induced mitotic arrest. As a key regulator of mitotic spindle assembly, Aurora A kinase was hyperphosphorylated in early mitosis under oxidative stress, which may disturb the function of Aurora A in mitotic spindle formation. Our findings identified a mechanism by which ROS regulate mitotic progression and indicated a potential molecular target for the treatment of oxidative stress-related diseases.
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