Fig. 6

YTHDF2 mediated the recognition and degradation of m6A-methylated XIST. a RIP assay confirmed the association between XIST and m6A reader protein YTHDF2 in CRC cells. GAPDH mRNA was used as a non-target control. ns, not significant, **, p < 0.01, ***, p < 0.001. b RNA pull-down assay confirmed XIST was specifically recognized by YTHDF2. EGFP RNA was used as RNA control. GAPDH was used as protein control. c Real-time PCR showed the level of XIST in control and shYTHDF2 CRC cells. *, p < 0.05. d Negative correlation of METTL14 and XIST expression in CRC tissue from our center (right panel) or from TCGA public dataset (left panel). R and p values were as indicated. e The expression levels of XIST in shYTHDF2 and control cells were quantified by real-time PCR at indicated time points after actinomycin D treatment and the decay rate of XIST was evaluated with a linear regression model. *, p < 0.05. f Summary of the mechanism by which METTL14 regulates the malignant phenotype of CRC. Data were presented as the mean ± SD of at least three independent experiments. P values were determined by Student’s t-test