Fig. 6
Knocking out GLUT1 in A549 cells did not decrease xenograft tumor growth. CRISPR–Cas9-mediated GLUT1 gene knockout was characterized by different assays. A549GLUT1KO tumors were generated and grown in nude mice to determine their growth rate. Values shown are mean ± SEM. *P < 0.05, **P ≤ 0.01, and ***P ≤ 0.001. a Western blot confirmation for GLUT1 protein knockout in A549 cells. b A549GLUT1KO cells reduced basal glucose uptake capacity compared with A549WT cells. c Images of tumors generated from WT and A549-GLUT1KO cells after 4 weeks of growth. Top row: A549GLUT1KO tumors, bottom row: A549-WT tumors. d Tumor volumes (mm3) after 4 weeks of growth. e Tumor weights (g) after 4 weeks of treatment. f Relative glucose intracellular glucose levels in A549 WT and A549 GLUT1KO cells treated with or without DRB18. G. DRB18 reduced cell viability in A549 WT and GLUT1KO cells after 72 h of treatment in a dose-dependent manner in a resazurin assay. h A hypothetical model for the mechanism of action of DRB18 showing it reducing glucose uptake via glucose transporters targeting glucose-based metabolism in cancer cells ultimately leading to cell death