Fig. 5

METTL3 promotes glycolysis and the colony-forming ability of breast cancer cells. a The ECAR in the METTL3 KO group and control group of MCF-7 cells in response to glucose, oligomycin and 2-DG, * p < 0.05. b The levels of glycolysis, glycolysis reserve and glycolysis capacity in MCF-7 cells compared with the control cells after deleting the expression of METTL3, n = 3, *** p < 0.001. c RNA-pull down assay showing the interaction between METTL3 and LATS1 mRNA. d The m6A level of LATS1 mRNA when the expression of METTL3 was altered in MCF-7 cells, as detected by MeRIP-qPCR, n = 3, ** p < 0.01. e The m6A level and METTL3 binding level of LATS1 mRNA when the m6A methylation sites on LATS1 mRNA were mutated in MCF-7 cells detected by MeRIP-qPCR, n = 3, *** p < 0.001. (f) Rescue of the expression of LATS1 by knocking out the expression of METTL3 and siRNA of LATS1 remarkably affected the proliferation of MCF-7 cells, n = 3, ** p < 0.01, *** p < 0.001. g Rescue of the expression of LATS1 by METTL3 significantly restored glycolysis in MCF-7 cells, *** p < 0.001