The cell cycle is marked by dynamic fluctuations in reactive oxygen species (ROS). While low levels of ROS can stimulate cell proliferation, excessive ROS lead to cell cycle arrest. Notably, cell cycle arrest can further generate more ROS, creating a bidirectional relationship that underscores the necessity for cells to finely tune ROS levels to maintain homeostasis and ensure proper cell cycle progression. Unlike classical cell cycle checkpoint systems, ROS directly oxidise cysteine residues in critical cell cycle regulators, with examples ranging from cyclins and cyclin-dependent kinases to APC/C, CDK inhibitors, and other CDK regulators, altering their functions. This review explores the interplay between ROS and the cell cycle, emphasizing how understanding their relationship could enhance therapeutic outcomes.
Hsiu et al. (Mon,) studied this question.