Fig. 6

NCAPG enhances the phosphorylation of PTEN through CKII. A A Co-IP assay showed that endogenous NCAPG and PTEN did not bind directly. B Co-IP assay of endogenous NCAPG and CKII in MHCC97H and HCCLM3 cells. CKII was detected in the immunoprecipitate when the anti-NCAPG antibody was used as bait. C NCAPG was detected in the immunoprecipitate when the anti-CKII antibody was used as bait. D Western blot analysis showing the levels of PTEN, p-PTEN and CKII when NCAPG was upregulated or knocked down. Quantitative analysis showed the same pattern. E TBB was added to NCAPG-overexpressing cells, and Western blot analysis showed that the levels of PTEN, p-PTEN and CKII were reversed. F Transfection with the CKII overexpression plasmid combined with NCAPG silencing. Western blotting was used to measure the levels of PTEN, p-PTEN and CKII, and it was found that the levels of PTEN, p-PTEN and CKII were reversed. G to J The proliferation ability of HCCLM3 and MHCC97H cells was reversed when TBB was added to NCAPG-overexpressing cells, as determined by EdU incorporation and CCK-8 assays. The values indicate the mean ± SD of three independent experiments (*P < 0.05, **P < 0.01, ***P < 0.001; independent Student’s t test). K to N The proliferation ability of HCCLM3 and MHCC97H cells, as determined by EdU incorporation and CCK-8 assays, was reversed when NCAPG was silenced and CKII was upregulated. The values indicate the mean ± SD of three independent experiments (*P < 0.05, **P < 0.01, ***P < 0.001; independent Student’s t test)