Fig. 3: Ectopic expression of GLUT1 rescued the defective tumorigenesis of HCC cells after MTR4 silencing.
From: MTR4 drives liver tumorigenesis by promoting cancer metabolic switch through alternative splicing
a Ectopic expression of GLUT1 in control and MTR4 KD cells was analyzed for MTR4 and GLUT1 by western blotting. Representative data from two independent experiments are shown. b, c ECAR in control cells and MTR4 KD cells transfected with either empty vector (EV) or plasmids expressing GLUT1 (GLUT1 OE) in response to glucose, oligomycin, and 2-DG. Data are presented as mean value ± s.d., two-way ANOVA with a Tukey’s multiple comparison test. n = 3 independent experiments for each group. d The proliferation of indicated cells were analyzed with CCK8 assay. Data are presented as mean value ± s.d. Two-way ANOVA with a Tukey’s multiple comparison test. n = 3 independent biological samples. e The weight of tumors formed by indicated cells in NSG mice was measured and compared. Data are presented as mean value ± s.d. One-way ANOVA, followed by Bonferroni post-tests. n = 8 independent biological samples for each group. p value is indicated. Source data are provided as a Source Data file.
