Fig. 3: METTL16 silencing affects crucial pathways involved in AML survival and perturbs the m6A epitranscriptome of leukemic cells.
From: METTL16-mediated inhibition of MXD4 promotes leukemia through activation of the MYC-MAX axis
A Pie chart showing the percentage of upregulated and downregulated genes following METTL16 suppression compared to SCR in K562 cells (Log2FC > 1; P < 0.05). RNA-seq was carried out after 4 days of puromycin selection. B GSEA showing the top differential hallmark gene sets (P < 0.05) associated with shMETTL16 and SCR cells (NES indicates the normalized enrichment score). C GSEA analysis showing the “MYC targets” and “apoptosis” hallmark gene sets in (1) shMETTL16- (P < 0.01 and FDR < 0.01) and (2) SCR- transduced K562 cells (P < 0.01 and FDR < 0.01). D Scatter plot depicting the log2 fold changes methylation gene sites in SCR (x-axis) versus shMETTL16 (y-axis). Methylation in 5′ UTR of MXD4 and exon 6 of MXD1 have been highlighted. E Integrative Genomics Viewer (IGV) visualization of m6A peak at the 5’UTR region of MXD4 in SCR and shMETTL16 samples (P < 0.01). F GO analysis of hypomethylated and upregulated genes following METTL16 depletion. Significant enrichment was defined using an unadjusted p value.
