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. 2024 Feb 24;15(2):170. doi: 10.1038/s41419-024-06544-6

Fig. 3. PRMT1-mediated meR206-PGK1 promotes colorectal cancer cell glycolysis by facilitating ERK-mediated PGK1-Ser203 phosphorylation.

Fig. 3

A–C The spatial positions of Serine 203 and arginine 206 in PGK1 were predicted (A). The changes of pS203-PGK1 and meR206-PGK1 by IP of Flag, and the interaction between PGK1 and ERK were detected both in HCT116 cells (B) and HEK293T (C) cells when wild and mutant Flag-PGK1 (WT, R206K) were transiently overexpressed. D, E The amount of pS203-PGK1 and the PGK1-ERK interaction were detected by IP Flag-PGK1 after over-expressing PRMT1 (D) or silencing PRMT1 (E) in HCT116 cells, respectively. F Confocal detected the mitochondrial localization of PGK1 in wild and mutant Flag-PGK1 (WT, R206K) HCT116 cells. G–L Glucose uptake (G, H), lactate production (I, J), and extracellular acidification rates (ECAR) (K, L) were analyzed in stable overexpressed wild and mutant Flag-PGK1 (WT, R206K) HCT116 cells and LOVO cells. Data are represented as mean ± SEM of three independent experiments, and **p < 0.01, ***p < 0.001 (Student’s t-test).