Fig. 8: Proposed model of the role of DAB2IP’s phosphorylation in SAC maintenance and cancer development suppression.

Cdk1 phosphorylates DAB2IP on its central region during mitosis. This phosphorylation provides a docking position for PLK1 and, meanwhile, activates the kinase activity of PLK1 and its downstream Mps1 kinase to promote the initiation of the MCC. Loss of expression or Cdk1-mediated phosphorylation of DAB2IP leads to a weakened SAC and increases chromosome missegregation and aneuploidy, which contributes to tumorigenesis and chemoresistance.