Fig. 6

ADPGK regulates PCa glycolysis through AMPK phosphorylation. Effect of ADPGK overexpression on AMPK and p-AMPK protein expression levels in 22Rv1 (a) and PC3 (b) cells. c Effect of ADPGK knockdown by siRNA on AMPK and p-AMPK protein expression levels in LNCaP cells. d Effect of the ADPGK inhibitor 8-Bromo-AMP on AMPK and p-AMPK protein expression levels in 22Rv1 cells. e ECAR test in ADPGK OE and ADPGK OE + 10 μmol/L Compound C (a type of AMPK inhibitor) in PC3 cells (n = 4). f CCK-8 assay showed the cell viability changes after ADPGK overexpression and Compound C addition (10 μmol/L) (n = 7). g ECAR results of siADPGK#3 and siADPGK#3 + 0.5 mmol/L acadesine (AICAR, a type of AMPK agonist) in LNCaP cells (n = 3). h CCK-8 assay showed the cell viability changes after ADPGK knockdown and AICAR addition (0.5 mmol/L) in LNCaP cells (n = 5). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns non-significant. PCa prostate cancer, ADPGK ADP-dependent glucokinase, AMPK AMP-activated protein kinase, NC negative control, OE overexpression, ECAR extracellular acidification rate, 2-DG 2-deoxy-glucose, AICAR acadesine, OD optical density, SD standard deviation, a.u. artificial unit