Fig. 1: PRMT1 enhances colorectal cancer cell glycolysis.
From: PRMT1-mediated PGK1 arginine methylation promotes colorectal cancer glycolysis and tumorigenesis
A–L The glucose uptake kit and lactate production kit were used to analyze the glucose uptake and lactate production when PRMT1 was overexpressed (A–D) or knocked down (E–H) in HCT116 cells and DLD1 cells or when HCT116 and DLD1 cells were treated with GSK3368715 (3.1 nM, 48 hours) (I–L). M–O Extracellular acidification rates (ECAR) were analyzed when PRMT1 was stable overexpressed (M), knocked down (N) in HCT116 cells or when HCT116 cells were treated with GSK3368715 (O) by Seahorse Bioscience Extracellular Flux Analyzer. The working concentration of the drugs showed in M–O was Glucose (10 μM), Oligomycin (1 μM), and 2-DG (50 μM). GSK3368715 treatment: 3.1 nM for 24 h. Data are represented as mean ± SEM of three independent experiments, and *p < 0.05, **p < 0.01, ***p < 0.001 (Student’s t-test).
