Abstract
In responding to DNA damage, cells may trigger checkpoint controls to arrest cell cycle progression at G1 or G2/M phase to prevent the injured DNA to enter S phase or mitosis. Although the checkpoint control in general consists of DNA damage sensors, signal transducers and effectors, the detailed mechanisms of checkpoint controls may be varied due to the differences of cell stages, DNA damages or cell types. Chinese hamster ovary cells (CHO-K1) which fail to arrest at G1 phase following UV irradiation through the absence of p21 provide a simplified system to investigate the molecular mechanism of UV-induced cell cycle arrest. In our study, we found that CHO-K1 underwent apoptosis under high dose of UV irradiation, while arrested at G2/M phase under low dose of irradiation. The G2/M arrest was abolished by caffeine and the cells underwent massive apoptosis. Moreover, the G2/M arrest is regulated by p53-independent fashion through Chk1-Cdc25C signaling pathway. Furthermore, the cell cycle progression was restored and UV-induced DNA damages were completely repaired in cells with G2/M arrest. The present study clearly show the role of G2/M arrest in giving CHO-K1 cells enough time to repair DNA adducts, and protecting the cells from UV-induced apoptosis.