Fig. 7

ALKBH5-catalyzed demethylation of FOXP2 represses its expression. A, The m6A modification site of FOXP2 was analyzed using the SRAMP tool. B, Volcano plots of m6A modification differences between OC and control tissues in the GSE119168 and GSE196748 datasets. C, The interactions between FOXP2 mRNA and ALKBH5 protein predicted in the RNAINTER database. D, Correlation between ALKBH5 expression in OC and patients’ survival in the Kaplan-Meier Plotter database. E, The m6A modification of FOXP2 in tumor tissues and adjacent tissues (n = 19) of OC patients was assessed using MeRIP-qPCR. F, Expression of ALKBH5 in tumor tissues and adjacent tissues of OC patients (n = 19) detected by immunohistochemistry. G, ALKBH5 mRNA expression in A2780 and SKOV3 cells following infection with lentiviral vectors packaged with ALKBH5 knockdown was evaluated using RT-qPCR. H, FOXP2 and CEP55 mRNA expression in A2780 and SKOV3 cells following infection with lentiviral vectors packaged with ALKBH5 knockdown was evaluated using RT-qPCR. I, Effect of knockdown of ALKBH5 on m6A modification of FOXP2 analyzed by MeRIP-qPCR. J, The binding relation between ALKBH5 and FOXP2 mRNA was analyzed using RIP-qPCR. K, The effect of knockdown of ALKBH5 on FOXP2 mRNA stability was evaluated using actinomycin D-mediated RNA half-life assay. L, The effect of knockdown of ALKBH5 on luciferase activity was assessed using a dual-luciferase reporter assay. Statistical significance was assessed using an unpaired t-test or ANOVA. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. All cell experiments were repeated three times