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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

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

Fig. 3

Association between m6A and ENO1 and the link with clinical outcome. (A) Venn diagram of proteomics showing candidates that were elevated in LUAD and upregulated by m6A. (B) ENO family expression and m6A levels in H1975 and H1299 cells with indicated treatment, as measured by IB and dot blot, respectively. (C) ENO1 activity in H1975 and H1299 cells with different treatments, as indicated. (D) Correlation between global m6A and ENO1 in LUAD. (E) The percentage of LUAD expressing different levels of ENO1 in those with different tumor/adjacent global m6A ratios. (F-H) IHC (F), heatmap (G) and IB (H) showing Eno1 expression in spontaneous LUAD from indicated KP-based mice. In panel G, the average levels of Eno1 in 20 fields of view are shown. Scale bar, 100 μm. (I-J) The percentage of patients at different stages in cohort #1 with different levels of global m6A (I) and ENO1 (J). (L-M) Overall survival of LUAD patients with high and low levels of ENO1, as analyzed from the data from Kaplan-Meier Plotter database (L) and our own (M) by log-rank test. Statistical analysis was performed using one-way ANOVA (C) and Chi-squared test (E, I, J). Data are presented as means ± SEMs from three independent experiments (C). **p < 0.01 indicates statistical significance

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