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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: The essential roles of m6A RNA modification to stimulate ENO1-dependent glycolysis and tumorigenesis in lung adenocarcinoma

Fig. 4

M6A-dependent regulation of glycolysis and 3D-spheroid formation via ENO1.Schematic representation of glycolysis processes. (B-E) The 2-PGA (B), PEP (C), Pyruvate (D) and ATP (E) levels in LUAD tissues with low or high global m6A levels. (F-H) ENO1 activity (F), PEP (F), glucose uptake (F), lactate production (F), ATP (F), ECAR (G) and OCR (H) in the presence or absence of METTL3 knockout and ALKBH5 overexpression, with or without ENO1 compensation in H1975 cells, as indicated. (I-K) ENO1 activity (I), PEP (I), glucose uptake (I), lactate production (I), ATP (I), ECAR (J) and OCR (K) in control and ENO1-/- H1299 cells with or without ALKBH5 knockout and METTL3 overexpression. (L) 3D-spheroid formation that generated from H1975 cells with or without METTL3 knockout and ALKBH5 overexpression, in the presence or absence of compensation for ENO1. Scale bar, 100 μm. (M) 3D-spheroid formation that generated from control and ENO1-/-H1299 cells with or without ALKBH5 knockout and METTL3 overexpression. Scale bar, 100 μm. Statistical analysis was performed using t test (B-E), one-way ANOVA (F, I, L, M) and two-way ANOVA (G, H, J, K). Data are presented as means ± SEMs from indicated samples or three independent experiments. **p < 0.01 indicates statistical significance and N.S. indicates no significance

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