Figure 9: CD24 is required for viral oncogene-mediated inactivation of p53 function. | Nature Communications

Figure 9: CD24 is required for viral oncogene-mediated inactivation of p53 function.

From: Intracellular CD24 disrupts the ARF–NPM interaction and enables mutational and viral oncogene-mediated p53 inactivation

Figure 9

(a) By increasing the overall levels of p53 protein, Cd24 silencing increases the proportion of SV40 T antigen-unbound p53. SV40 T antigen was tagged with Flag and introduced into the mouse prostate cancer cell line C3 with or without transduction of CD24 shRNA. The total cellular (left panel) or SV40 T antigen-associated or non-associated p53 (right panel) were determined by either western blot or anti-Flag immunoprecipitation followed by western blot. Note that CD24 was not co-precipitated. S: supernatant; P: pellet. (b) Cd24 silencing reveals p53 function in SV40 large T antigen (SV40 Tag)-transduced (top) and human papilloma viral protein E6 (HPV E6)-transduced C3 cells (bottom). SV40 Tag- or HPV E6-transduced C3 cells were transfected with WT or p53-binding site mutant p21 promoter linked with a luciferase reporter. The function of the endogenous Cd24 and Tp53 locus was confirmed by shRNA silencing of either genes. Data shown are means and s.d. of relative luciferase activity. (c) In the Tp53+/+ TRAMP model, targeted mutation of Cd24 increased the levels of p53 and p21. Data shown are photographs of immunohistochemical analysis of p21 and p53 levels from either Cd24+/+ or Cd24−/− prostate cancer samples. (d) Cd24 silencing increases the proportion of HPV E6-unbound p53, as in a, except that HPV E6 was used instead of SV40 TAg. All data in this figure have been reproduced two or three times. Co-IP, co-immunoprecipitation; Mut, mutant; WB, western blot.

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