Fig. 3

Inhibition of ADPGK suppresses PCa progression in vitro. a RNAi-mediated ADPGK knockdown was validated by qPCR. b RNAi-mediated ADPGK knockdown was validated by Western blotting. c Cell proliferation was measured by EdU assay after ADPGK knockdown (n = 3). Scale bar = 50 μm. d CRISPR/Cas9-mediated ADPGK knockdown was validated by Western blotting. e The effect of ADPGK knockdown on cell proliferation was validated in a colony formation assay (n = 3). f The effect of ADPGK knockdown on PCa cell migration ability was validated in a wound healing assay (n = 3). Scale bar = 200 μm. g A CCK-8 assay was performed to evaluate the effect of an ADPGK inhibitor (8-Bromo-AMP) on PCa cells (n = 5). h An EdU flow cytometric assay was performed in 22Rv1 cells using different concentrations of 8-Bromo-AMP (n = 3). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns non-significant. Scr scramble, PCa prostate cancer, SD standard deviation, NC negative control, ADPGK ADP-dependent glucokinase, qPCR quantitative polymerase chain reaction, CRISPR clustered regularly interspaced short palindromic repeats, a.u. artificial unit