Fig. 5

Down-regulated TRIM38 depended on GLUT1 to drive glycolytic process and tumor progression. a–c Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay, in which GLUT1 knockdown suppressed the growth of TRIM38-deficient cells. d TRIM38 knockout enhanced T24 cells anchorage-independent growth in soft agar, which could be notably suppressed by TRIM38 overexpression (scale bars = 200 µm, left panel). Quantification of the soft agar colony formation assay results (right panel). e Knockout of TRIM38 significantly promoted glucose uptake, which could be restored by GLUT1 inhibition. f T24 cells (Ctrl & TRIM38-KO#1) with a Seahorse XF24 analyser for 100 min were used to depict the ECAR profiles. The metabolic inhibitors were injected sequentially at different time points as indicated. g EJ cells (Ctrl & TRIM38) with a Seahorse XF24 analyser for 100 min were utilized to show the ECAR profiles. The metabolic inhibitors were injected sequentially at different time points as indicated