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. 2022 Feb 22;12(4):1825–1839. doi: 10.1016/j.apsb.2022.02.014

Figure 3.

Figure 3

GAPDH inactivation by osimertinib reduces aerobic glycolysis in TECs. (A) Comparison of ECAR in CD45–CD31+ endothelial cells from transplanted CT26 tumors after treatment of mice with osimertinib (1 mg/kg) or vehicle daily for 14 days by oral gavage. (B) Quantification of sequential compound injections measuring glycolysis, glycolytic capacity, glycolytic reserve and non-glycolytic acidification as shown in (A). (C) HUVECs were treated with osimertinib or DMSO for 24 h after overexpression with GAPDH vector for 24 h. Glycolytic intermediates were measured from lysates via LC–MS/MS. Heat map showed the blockade of the glycolytic flux at the level of GAPDH. (D) Lactate levels of HUVECs treated as indicated in (C). (E) Glycolysis was measured via Seahorse extracellular flux analyzer in HUVEC as indicated treatment. (F) Quantification of glycolysis, glycolytic capacity, glycolytic reserve and non-glycolytic acidification as shown in (E). Statistical analysis by unpaired Student's t-test or one-way ANOVA. Data are presented as mean ± SEM (n = 5). G6P, glucose-6-phosphate; F6P, fructose-6-phosphate; GAP, glyceraldehyde-3-phosphate; DHAP, dihydroxyacetone phosphate; 3PG, 3-phosphoglycerate; 2PG, 2-phosphoglycerate and PEP, phosphoenolpyruvate.