type cells, Wip1-depleted HCT116 p53−/− cells were able to recover from G2 arrest, indicating that activated p53 in Wip1-depleted cells caused the failure to recover from G2 arrest. Specifically, the authors showed that Wip1 inhibits the transcriptional repression of target genes, specifically Cyclin B1, by p53 (76). Therefore, Wip1 plays a critical role through p53 to facilitate checkpoint recovery. Furthermore, the authors concluded that this may be another mechanism by which Wip1 promotes tumorigenesis – by maintaining the ability of a cell to proliferate during oncogenic stress (76).
