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. 2024 Oct 9;10:431. doi: 10.1038/s41420-024-02202-0

Fig. 6. METTL3-156aa promotes macrophage glycolysis by binding to LDHA.

Fig. 6

A–C Lactate levels of THP1 cell supernatants after knockdown of circMETTL3 (A), overexpression circMETTL3 (B) or addition of METTL3-156aa (C). Data are shown as mean ± SD (n = 3 independent experiments, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). D, E Mutual interaction of LDHA and Flag-METTL3–156aa in HEK293T (D) and THP-1 (E) cells were determined by IP. F Flag-tagged METTL3–156aa was transfected into HEK293T cells and immunofluorescence was performed using anti-Flag and anti-LDHA antibody. Scale bar: 20x, 20 μm; 63x, 10 μm. All experiments were repeated at least three times. G The in situ PLA was performed to examine the interaction between LDHA and METTL3-156aa (scale bar, 10 μm). All experiments were repeated at least three times. H Enhanced levels of METTL3-156aa binding to LDHA after transfection of circMETTL3 vector in HEK293T cell line. I–N The ECAR was determined using a Seahorse XF96 analyzer to evaluate glycolytic flux after overexpression circMETTL3, knockdown of circmettl3, or addition of METTL3-156aa. Glycolysis, glycolytic capacity, and glycolytic reserve were determined by the sequential addition of 10 mM glucose, 1 mM oligomycin, and 50 mM 2-D-glucose. Values represent the mean ± SD of at least three independent experiments (*p < 0.05, **p < 0.01, ***p < 0.001).