Fig. 4: m6A loss following METTL16 KD increases RNA stability of MXD4 and suppresses MYC activity.
From: METTL16-mediated inhibition of MXD4 promotes leukemia through activation of the MYC-MAX axis
A METTL16 RIP assay showing MXD4 RNA enrichment in K562 cells (n = 3) (*P < 0.05). B Actinomycin D assay showing MXD4 expression at indicated time points in SCR, shMETTL16.1, and shMETTL16.2 K562 cells (n = 3) (*P < 0,05). C WB analysis of MXD4 in SCR-, shMETTL16.1-, and shMETTL16.2-transduced K562 cells (n = 3). D WB analysis showing MXD4 protein levels following 48 h treatment with METTL16i (n = 3). E IP of MAX in shSCR and shMETTL16 transduced K562 cells at 5 days post-infection (n = 3). Immunoblot was performed with the indicated antibodies. F RT-qPCR showing expression of the indicated genes in SCR, shMETTL16.1, and shMETTL16.2 cells at 5 days post -infection (n = 3) (***P < 0.001; **P < 0.01). G RT-qPCR showing expression of the indicated genes following 48 h treatment with METTL16i (n = 3) (***P < 0.001; **P < 0.01). One-way analysis of variance (ANOVA), non-parametric, was used to calculate the statistical significance of SCR vs shMETTL16.1 and SCR vs METTL16.2 in (B, F), and NT vs CDH24-20, NT vs CDH24-21 in (G); Student’s t test was used in (A).
