Fig. 4

Inhibition of CCDC106 phosphorylation suppresses CCDC106-dependent degradation of the p53 protein. a and b The influence of wild-type and mutant CCDC106 on p53 protein expression levels. HA-p53 was cotransfected with an equal (a) or an increasing (b) amount of wild-type or mutant Myc-CCDC106 plasmid into HEK293 cells, and cell lysates were prepared and subjected to WB using anti-HA and anti-Myc antibodies at 24 h posttransfection. c The influence of wild-type and mutant CCDC106 on the expression levels of p53 and its targets. Cell lysates were extracted from SiHa and HBL100 cells stably expressing empty vector, CCDC106 or S130/147A mutant CCDC106, and subjected to WB. d The influence of CX-4945 treatment on the expression levels of p53 and its targets. Cells were treated with increasing concentrations of CX-4945 and harvested for WB analysis 24 h after treatment. e The influence of CX-4945 treatment on the expression of HA-p53 fusion protein. HA-p53 plasmid was cotransfected with empty vector or Myc-CCDC106 plasmid into HEK293 cells. Then, the cells were treated with CX-4945 for 24 h. HA-p53 fusion protein expression levels were analyzed by WB using an anti-HA antibody. f Silencing CCDC106 significantly reduces the effect of CK2β overexpression on p53 stability. HeLa cells were cotransfected with CK2β and siRNA targeting CCDC106 or CK2β, and harvested for WB analysis at 24 h posttransfection