Fig. 7From: The essential roles of m6A RNA modification to stimulate ENO1-dependent glycolysis and tumorigenesis in lung adenocarcinomaClinical and translation significance of the study.(A-B) ENO1 and YTHDF1 protein expression in adjacent and matched-tumor tissues from LUAD patients of cohort #1 (n=192). (C-E) Correlations between METTL3 and ENO1 (C), ENO1 and global m6A (D), and between ALKBH5 and ENO1 (E) in cohort #1. The protein and m6A levels were calculated as the ratios between that from tumor and matched-adjacent tissues. (F-J) ENO1 (F), YTHDF1 (G), METTL3 (H), global m6A level (I) and ALKBH5 (J) in LUAD with indicated tumor stages from cohort #3 (n=20/group). (K-M) CDX that generated by H1299 cells with or without combined ALKBH5 knockout and METTL3 overexpression followed by administrating mice with DMSO, DAA (50mg/kg), 2DG (1000mg/kg) or ENOblock (20mg/kg). The global m6A levels (K), representative images of xenografts (K), tumor volume (L) and mice weights (M) were graphed and shown (n=6/group). Scale bar, 1cm. (N-P) PDX mice models with high and low global m6A levels were administrated with DMSO, DAA (50mg/kg), 2DG (1000mg/kg) or ENOblock (20mg/kg). The global m6A levels (N), representative images of xenografts (N), tumor volume (O) and mice weight (P) were graphed and shown. (n=6/group). Scale bar, 1cm. (Q-R) Representative H&E images of spontaneous LUAD in KPE mice following being infected with AVV5 expressing Cre and administrated with DMSO, DAA (25mg/kg), 2-DG (500mg/kg) or ENOblock (10mg/kg), as indicated (Q). The overall survival curves for KPE mice with established LUAD following drug administration are also shown in panel P R (n=6/group). Statistical analysis was performed using t test (A, B, K, N), spearman rank-correlation analysis (C-E), one-way ANOVA (F-J, M, P), two-way ANOVA (L, O) and log-rank tests (R). Data are presented as means ± SEMs from indicated samples. **p < 0.01 indicates statistical significance and N.S. indicates no significanceBack to article page