Fig. 2
From: Aspirin reprogrammes colorectal cancer cell metabolism and sensitises to glutaminase inhibition
Long-term aspirin treatment reprogrammes nutrient utilisation in CRC cells. a Extracellular flux analysis of long-term (52 weeks) 2-mM and 4-mM aspirin-treated SW620 cells compared to controls. Error bars represent SEM (n = 3 independent experiments). ns = not significant (p > 0.05 following t tests at indicated time points). b, c Schematics of U-[13C]-Glc (b) and U-[13C]-Q (c) incorporation into TCA cycle metabolites and amino acids. Created with BioRender.com. d–j SIL data for long-term (52 weeks) 4-mM aspirin-treated SW620 cells compared to control cells. Error bars represent SD (n = 3 technical replicates). Asterisks refer to p values obtained from t tests at the 8-h time point (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). d, e Proportion of 13C labelling in citrate, glutamate and malate from U-[13C]-Glc and U-[13C]-Q over time. f, g Proportion of 13C labelling in metabolite pools at 8 h from U-[13C]-Glc (f) and U-[13C]-Q (g). Asterisks indicate the adjusted p value obtained using multiple t tests. h, i Mass isotopomer distribution (MID) analysis at 8 h for U-[13C]-Glc (h) and U-[13C]-Q (i) labelling in citrate, glutamate and malate. Asterisks indicate the adjusted p value obtained using multiple t tests. j Ratio of m + 5 glutamateo m + 5 glutamine in long-term 4-mM aspirin-treated cells in comparison to control at 8 h from U-[13C]-Q