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. Author manuscript; available in PMC: 2020 May 15.
Published in final edited form as: Cancer Res. 2019 Mar 18;79(10):2748–2760. doi: 10.1158/0008-5472.CAN-18-2799

Fig. 6.

Fig. 6.

Impact of HK2-ASO1, DPI, MET, and PER on HK1−HK2+ OPM2 cell metabolism. Effects of HK2-ASO1, DPI, MET and PER, alone and in combination for 24 h on OPM2 (A) glucose consumption and lactate production, and (B) cellular ATP/(AMP+ADP) ratios. (C) OPM2 cell viability after 24 h treatments with HK2-ASO1, DPI, MET and PER, alone and in combination, determined by trypan blue staining. No significant differences could be detected between the vehicle control and any of the experimental treatment groups. (D) Effects of HK2-ASO1, DPI, MET and PER, alone and in combination for 24 h, on the levels of 129 important metabolites in OPM2 cells. (E) Effects of 24 h treatments with HK2-ASO1/DPI/PER and HK2-ASO1/MET/PER on relative changes in cellular pool sizes of amino acids, TCA cycle metabolites, fatty acid intermediates, purines and pyrimidines in OPM2 cells. (F) Effects of 24 h treatments with HK2-ASO1/DPI/PER and HK2-ASO1/MET/PER on relative changes in 13C portions of amino acids, TCA cycle metabolites, purines and pyrimidines in OPM2 cells.