Camptothecin induces G₂/M phase arrest through the ATM-Chk2-Cdc25C axis as a result of autophagy-induced cytoprotection: Implications of reactive oxygen species.

ABSTRACT: In the present study, we report that camptothecin (CPT) caused irreversible cell cycle arrest at the G₂/M phase, and was associated with decreased levels of cell division cycle 25C (Cdc25C) and increased levels of cyclin B1, p21, and phospho-H3. Interestingly, the reactive oxygen species (ROS) inhibitor, glutathione, decreased CPT-induced G₂/M phase arrest and moderately induced S phase arrest, indicating that the ROS is required for the regulation of CPT-induced G₂/M phase arrest. Furthermore, transient knockdown of nuclear factor-erythroid 2-related factor 2 (Nrf2), in the presence of CPT, increased the ROS' level and further shifted the cell cycle from early S phase to the G₂/M phase, indicating that Nrf2 delayed the S phase in response to CPT

SUBMITTER: Prasad Tharanga Jayasooriya RG 

PROVIDER: S-EPMC5955160 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature