Fig. 4
TKT sustains the ratios of NADPH/NADP and GSH/GSSG and enhances viability in response to oxidative stress in HCC cells. a TKT activity in TKT knocking-down cell lines (HCCLM3). b TKT activity in TKT and TKT enzyme-inactivating mutant overexpression cell lines (Huh7). c The glucose consumption rate of TKT knocking-down cell lines (HCCLM3). d The glucose consumption rate of TKT and TKT enzyme-inactivating mutant overexpression cell lines (Huh7). e NADPH/NADP ratio in TKT knockdown cell lines (HCCLM3). f GSH/GSSG ratio in TKT knockdown cell lines (HCCLM3). g TKT knockdown inhibited the viability of HCCLM3 cells under oxidative stress by treatment with 3 mM H2O2, even when TKT enzymatic activity was inhibited by 0.5 mM Oxythiamine (OT). h TKT overexpression (not only wild-type TKT, but also the TKT-D155A enzyme-inactivating mutant) increased the viability of Huh7 cells under oxidative stress by treatment with H2O2. i Relative PPP/Glycolysis Flux. j Overview of isotopomer formation through carbon flux distribution of [1,2-13C2]-glucose. The figure showed lactate labeling when1,2-13C2 glucose is metabolized through glycolysis directly or fed back through the PPP. Red circles correspond to 13C-labeled carbons, and black circles correspond to unlabeled 12C carbons (*: p < 0.05; **: p < 0.01)