Fig. 4
From: Targeting MYC-enhanced glycolysis for the treatment of small cell lung cancer
PFK158-treated MYCHigh cells do not increase oxidative respiration mechanisms. A Seahorse extracellular flux mito stress test monitored the oxygen consumption rate after the administration of oligomycin, FCCP, and rotenone and antimycin A. B Basal oxygen consumption is significantly reduced in H446 cells compared with DMS79. In H446 cells treated with PFK158, basal oxygen consumption is also significantly reduced compared with untreated cells. C Maximal oxygen consumption is significantly reduced in H446 cells compared with DMS79. In H446 cells treated with PFK158, maximal oxygen consumption is also significantly reduced compared with untreated cells. D Mitochondria-generated ATP is significantly reduced in H446 cells compared with DMS79. In H446 cells treated with PFK158, ATP is also significantly reduced based on untreated cells. E Proton leak is unchanged between DMS79 and H446 cells, but significantly reduced in H446 cells treated with PFK158. F Coupling efficiency is significantly reduced in H446 cells compared with DMS79. In H446 cells treated with PFK158, coupling efficiency is also significantly reduced compared with untreated cells. G Spare respiratory capacity is unchanged between DMS79 and H446 cells, but significantly reduced in H446 cells treated with PFK158. H Reactive oxygen species (ROS) generation is significantly increased in MYCHigh (H446, H524, H146, H211, H1048, H841) cells treated with PFK158 compared with MYCLow (DMS79, H196, H526, H345) cells. I The mitochondrial membrane potential is significantly reduced in MYCHigh (H446, H524, H146, H211) cells treated with PFK158 compared with MYCLow (DMS79, H196, H526, H345) cells. J There are no differences in mitochondrial content regardless of MYC status or treatment; MYCLow cell lines: DMS79, H196, H526; MYCHigh cell lines: H446, H524, H146, H211, H1048, H841, H82, H865 (*P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.001)