Fig. 2: Methylglyoxal is produced as a byproduct of glycolysis in NSCLC.
From: Reactive metabolite production is a targetable liability of glycolytic metabolism in lung cancer

a, b Schematic detailing how labeled carbon (denoted by blue circles) from [U-13C2]glycine (a) or [U-13C6]glucose (b) can be incorporated into methylglyoxal based on known pathways. c, d Isotopomer distribution of methylglyoxal in lung cancer cell lines (3553T3 and LGSP) independently derived from KP mice that were cultured for 24 h in the presence of [U-13C2]glycine (c) or [U-13C6]glucose (d). The isotopomer distribution was calculated using data shown in Supplementary Fig. 2a-b;d-e (n = 3). e Isotopomer distribution of methylglyoxal in autochthonous lung tumors arising in LA2 mice following a 6 h infusion of 30 mg/kg/min [U-13C6]glucose. Values were normalized to plasma enrichment of glucose and the isotopomer distribution was calculated using data shown in Supplementary Fig. 2g, h (n = 8). f Relative lactoylglutathione (LGSH) levels in 3553T3 and LGSP cells as detected by LCMS. Levels are shown for cells cultured in standard media, or media containing the indicated amount of 2-deoxyglucose (2DG) for 24 h. Values shown are the peak area of LGSH normalized to the peak area of reduced glutathione (n = 3). P values were calculated by unpaired, two-tailed t-test. g Correlation between LGSH abundance in samples derived from NSCLC patient samples as measured by LCMS, and the maximum standardized uptake value of (SUVmax) as measured by 18F-FDG-PET imaging (n = 24). Values in c–f denote mean ± SEM.