Fig. 5

DMAMCL suppressed aerobic glycolysis and decreased PFKL expression level in NB. After NGP and BE2 cells were treated with different DMAMCL concentrations for 24 h, ECAR was measured by adding glucose, oligomycin (ATP synthase inhibitors), and 2-deoxy-d-glucose (2-DG, hexokinase inhibitor) in turn to reflect the glycolysis rate including the glycolytic function, basal glycolysis, and glycolytic capacity, while extracellular glucose, extracellular lactate, and intracellular ATP levels were also measured. Glycolytic function, basal glycolysis, and glycolytic capacity of A NGP cells and B BE2 cells, ns (not significant): control vs DMAMCL treatment, *p < 0.05; **p < 0.01; ***p < 0.001. C Extracellular glucose concentration, D lactate excretion, and E intracellular ATP levels of NGP and BE2 cells. F PFKL, PKM2, and HK2 expression in NGP and BE2 cells after DMAMCL treatment for 0, 8, 16, and 24 h measured using western blotting. G PFKL expression in NGP and BE2 tumor tissues after DMAMCL treatment. *p < 0.05; **p < 0.01; ***p < 0.001