Fig. 5

CENPK interacts with SOX6 to activate Wnt signaling and inactivate p53 signaling in cervical cancer. a. TOP/FOP luciferase reporter assays were conducted for measuring the impact of CENPK and SOX6 on Wnt signaling activity. b. Co-immunoprecipitation analyses displaying the interaction between CENPK and SOX6. c. Immunofluorescence co-staining showing the colocalization of CENPK and SOX6. The red bars indicated by the arrows represent the colocalization of CENPK and SOX6. d. Co-immunoprecipitation analyses displaying the effect of CENPK knockdown on the interaction between CENPK and SOX6, and the impact of CENPK knockdown on the interplay between SOX6 and β-catenin. e. Immunofluorescence co-staining and cell fractionation assays showing the effect of CENPK on the expression and nuclear translocation of β-catenin and SOX6 in HeLa and SiHa cells incubated with lithium (30 nmol/L). f. Luciferase reporter assays were performed for elucidating the effect of CENPK and SOX6 on p53 signaling activity. g. Chromatin immunoprecipitation analyses were applied to estimate the impact of CENPK on SOX6-mediated c-Myc transcription. h. Cycloheximide chase assays assessing the impact of CENPK and SOX6 on p53 stability in HeLa cells. i. Co-immunoprecipitation analyses verifying the impact of CENPK and SOX6 on p53 ubiquitination in HeLa cells treated with MG132. j. Cell fractionation assays validating the impact of CENPK and SOX6 on p53 nuclear export in HeLa cells. Data are represented as the mean ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001; ns non-significant; IP immunoprecipitation; LiCl lithium