Fig. 3
From: Targeting MYC-enhanced glycolysis for the treatment of small cell lung cancer
MYCHigh cells are more glycolytic and sensitive to glycolysis inhibition. A Glucose uptake is higher in MYCHigh (H82, H446, H1048, H847) cell lines compared with MYCLow (DMS79, H345, H196, cell lines and is significantly decreased with PFK158 treatment. B RPM cells have higher glucose uptake compared with RP cells and is reduced with PFK158 treatment. C Similarly, extracellular lactate is higher in MYCHigh (H1930, H847, H524, H841, H446, H146, NJH29, H1048) cell lines compared with MYCLow (DMS79, H196, H526, H345, H2196, H1105) cell lines and reduced with PFK158 treatment. D Extracellular lactate is higher in RPM cell lines and reduced with PFK158 treatment. E Intracellular lactate significantly and positively correlates with LDHA expression (cell lines: NJH29, H1092, H446, H1436, H82, H1930, DMS79, H1048, H841, H526). F Glucose uptake in significantly lower in H446 cells treated with siRNA against MYC and PFKFB3 compared with a SCR negative control. G Extracellular lactate is significantly reduced in H446 cells treated with siRNA against MYC and PFKFB3 compared with a SCR negative control. H Based on the ECAR, glycolysis is significantly higher in the representative MYCHigh cell line H446 as compared with the representative MYCLow cell line DMS79. There were no changes in glycolysis in DMS79 cell treated with PFK158; however, glycolysis was significantly decreased in H446 cells treated with PFK158. I Acid produced by non-glycolytic pathways was significantly higher in DMS79 cells regardless of treatment. J The level of oligomycin-stimulated glycolysis indicative of forced glycolytic utilization is significantly lower in PFK158-treated H446 cells (*P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.001)