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Fig. 4 | Cancer & Metabolism

Fig. 4

From: Cancer cell metabolic plasticity allows resistance to NAMPT inhibition but invariably induces dependence on LDHA

Fig. 4

Enhanced glycolysis dependency of CEM RES cells. a Production of ATP from mitochondria and glycolysis were measured in CEM PA and CEM RES cells. Ratio of ATP production in the cytosol/mitochondria is shown. bf Metabolic enhanced towards glycolysis in CEM RES cells; CEM PA and CEM RES subclones at 10, 40, and 100 nM of FK866 were determined the aerobic metabolism, oxygen consumption (b), and ATP synthesis (c). Cells were analyzed in the presence of 5 mM pyruvate + 2.5 mM malate (P/M) or 20 mM succinate (Succ) to stimulate the pathways composed by complexes I, III, and IV or complexes II, III, and IV, respectively. To measure the glycolytic flux, glucose consumption (d), lactate production (e), and the activity of hexokinase (HK), 6-phospho-fructokinase (PFK), pyruvate kinase (PK), and lactate dehydrogenase (LDH) (f) were analyzed. gh CEM PA and CEM RES cells were treated with 2-deoxyglucose (g) and oligomycin A (h) for 48 h. Relative cell viability is shown. i Analysis of mitochondria content was conducted in CEM PA and CEM RES cells. Cells were exposed to mitotracker staining. FCCB was used as a negative control. Data was shown as mean ± S.D. of three independent experiments with technical triplicates, *p < 0.05, **p < 0.01, and ***p < 0.001

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