Fig. 5
Combined glycolysis and glutamine metabolism inhibitory drugs induce growth arrest in human cancer cell lines. a Proliferation curves of A549 (left panel) and HCT116 (right panel) incubated with BKM120 ( 
), CB-839 ( 
), or BKM120 + CB-839 ( 
) versus CTR ( 
), collected and counted at the indicated time points. b, c Untargeted metabolic analysis in A549 (b) and HCT116 (c) cancer cells. Hierarchical clustering heatmaps show significantly different intracellular metabolites in the four experimental conditions assessed by LC-MS and GC-MS. (p ≤ 0.05). d, e Mitochondrial respiration levels in A549 CTR ( 
) or under combinatorial treatments ( 
) (d), and in HCT116 CTR ( 
) or under combinatorial treatments ( 
) (e), under basal conditions or following the addition of oligomycin (1 μM), the uncoupler FCCP (1 μM) or the electron transport inhibitor Rotenone (0.5 μM) (n = 5). f, g Mitochondrial ATP level reflected by OCR levels in A549 (f) and HCT116 (g) CTR ( 
) or under combinatorial treatments ( 
), under basal conditions or following the addition of oligomycin (1 μM), the uncoupler FCCP (1 μM) or the electron transport inhibitor Rotenone (0.5 μM) (n = 5). h, i NADH/NAD+ ratio in CTR ( 
) or under combined treatment ( 
) in A549 (H) and HCT116 (I) based on relative abundance obtained by LC-MS analysis