Fig. 6: PRMT3 deficiency decreases GBM progression by inhibiting aerobic glycolysis.
From: PRMT3 drives glioblastoma progression by enhancing HIF1A and glycolytic metabolism

A Heatmap of the genes differentially expressed in control and PRMT3-KD U251cells after 72 hr. B Volcano plot of transcriptome profiles of wild-type and PRMT3-KD U251cells. Red and blue dots represent genes significantly upregulated or downregulated, respectively in PRMT3-KD cells compared to wild-type cells (fold change >1.5, p < 0.05). C KEGG analysis of the upregulated and downregulated genes in PRMT3-KD compared with wild-type U251cells. D GSEA enrichment plots of the glycolysis pathway, apoptosis and cell cycle pathway showing the comparison of gene expression profiles in wild-type U251cells and PRMT3-KD cells. NES, normalized enrichment score; p value, represents the statistical significance of the enrichment score. E Heatmap of the metabolites changed in PRMT3-KD GSC20 cells. F Relative levels of the metabolites in glycolysis/PPP, amino acid and nucleotide metabolism in Ctrl (red) and PRMT3-KD (blue) GSC20 cells. Data are presented as means ± SEM; n = 3 independent experiments; *p < 0.05; **p < 0.01; ***p < 0.001; two-tailed unpaired Student t-test. G ECAR was measured with a Seahorse XF96 Flux analyzer (left) and quantification (right) in Ctrl and PRMT3-KD GSC20 cells. *p < 0.05, **p < 0.01, ***p < 0.001. one-way ANOVA with multiple comparison test. H. OCR was measured with a Seahorse XF96 Flux analyzer (left) and quantification (right) in Ctrl and PRMT3-KD GSC20 cells. *p < 0.05, **p < 0.01, ***p < 0.001. two-tailed unpaired Student t-test. N.S., not significant.