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Oxidative stress induces mitotic arrest by inhibiting Aurora A-involved mitotic spindle formation

Guang-Fei Wang1, Qincai Dong2, Yuanyuan Bai2

  • 1Key Laboratory of Cell Proliferation and Regulation Biology, College of Life Sciences, Beijing Normal University, 19 Xinjiekouwai Avenue, Beijing 100875, China.

Free Radical Biology & Medicine
|December 27, 2016
PubMed

Insights

Reactive oxygen species (ROS) cause mitotic arrest by disrupting the mitotic spindle. This study reveals ROS-induced hyperphosphorylation of Aurora A kinase, a key regulator, impacting spindle formation and offering a target for oxidative stress diseases.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • Oxidative stress causes cellular damage, including DNA damage, cell cycle arrest, and apoptosis.
  • The precise mechanisms by which oxidative stress induces mitotic abnormalities remain unclear.

Purpose of the Study:

  • To elucidate the mechanism of oxidative stress-induced mitotic abnormalities.
  • To investigate the role of reactive oxygen species (ROS) in mitotic progression.
  • To identify potential molecular targets for treating oxidative stress-related diseases.

Main Methods:

  • Investigated the effects of exogenous and endogenous ROS on mitotic progression in cellular models.
  • Analyzed the formation and function of the mitotic spindle under oxidative stress conditions.
  • Examined the phosphorylation status and function of Aurora A kinase during mitosis under oxidative stress.

Main Results:

  • Exogenous and endogenous ROS were demonstrated to induce mitotic arrest.
  • ROS exposure led to delayed formation and abnormal function of the mitotic spindle, causing impaired mitosis and abnormal chromosome separation.
  • Aurora A kinase, a critical regulator of mitotic spindle assembly, was found to be hyperphosphorylated in early mitosis under oxidative stress, potentially disrupting its function.

Conclusions:

  • ROS-induced mitotic arrest is mediated by the disruption of mitotic spindle formation and function.
  • Hyperphosphorylation of Aurora A kinase is a key event in ROS-induced mitotic abnormalities.
  • Targeting Aurora A kinase may offer a therapeutic strategy for diseases associated with oxidative stress.
Keywords:
Aurora AMitotic arrestPhosphorylationROSSpindle

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