Fig. 1
Global m6A was modulated by METTL3 and ALKBH5 in LUAD.(A) Global m6A levels were measured by m6A methylation assay in tumor and matched-adjacent tissues from LUAD patients. (B) The percentage of LUAD in cohort #1 with distinct tumor/adjacent ratio of global m6A, as indicated. (C-D) METTL3 (C) and ALKBH5 (D) protein levels in tumor and matched-adjacent tissues from LUAD patients, as measured by ELISA. (E) IB of METTL3 and ALKBH5 in tumor and matched-adjacent tissues from 12 LUAD patients. (F-G) Correlation between global m6A and METTL3 (F), and between global m6A and ALKBH5 (G) in LUAD patients. The global m6A and protein levels were calculated as the ratios between tumor and matched-adjacent tissues. (H) The percentage of cases with different METTL3 and ALKBH5 expressions, as indicated, in LUAD with high global m6A levels. (I) The global m6A levels in different groups with indicated METTL3 and ALKBH5 expression from LUAD with high global m6A levels. (J) Global m6A levels in control and H1975 cells with separate or combined METTL3 knockout and ALKBH5 overexpression. (K) Global m6A levels in control and H1299 cells with separate or combined METTL3 overexpression and ALKBH5 knockout. (L-M) Percentage (L) and overall survival (M) of LUAD patients with different METTL3 and ALKBH5 expression, as indicated in cohort #2. Statistical analysis was performed using t-test (A, C, D), spearman rank-correlation analysis (F, G), one-way ANOVA (I-K) and log-rank test (M). Data are presented as means ± SEMs from indicated samples or three independent experiments. **p < 0.01, indicates statistical significance