Fig. 5

PRMT5 transcriptionally activated the expression of LDHA. A Fold change relative to control of glycolytic enzymes in HCT116 cells treated with or without tadalafil (TAD; 25 µM) for 24 h. Mean ± SEM of three independent experiments was shown. B Western blotting analysis to assess LDHA levels in HCT116, SW480, and Caco2 cells treated with or without JNJ-64619178 (JNJ; 0.5 μM). β-actin was used as loading control, and one representative experiment out of three is shown. C Expression of LDHA in CRC patients from GSE8671. D Survival analysis of LDHA in GSE17537 dataset. E Survival analysis of LDHA and PRMT5 in TCGA rectum adenocarcinoma. F % of cell proliferation of PRMT5-overexpressed HCT116 cells transfected with siNC or siLDHA was evaluated by MTT assay. Mean ± SEM of three independent experiments is shown. G The luciferase activity of LDHA promoter in EGFP (CTRL) and PRMT5-overexpressed HCT116 cells measured by dual luciferase reporter assay. H H3R8me2s binding to LDHA in PRMT5-overexpressed HCT116 cells treated with or without tadalafil (TAD; 25 µM) for 24 h measured by ChIP assay. *P < 0.05; **P < 0.01; ***P < 0.001; n.s., no significance