Fig. 6: EZH2 deficiency stabilizes a set of oncogenic transcripts through cytoplasmic ADAR1p110.

a The workflow of RNA-seq to measure the global change of RNA half-lives. b Box plot showing the RNA half-life in each indicated group based on the RNA-seq data (n = 2 for each group). P values were calculated by two-tailed unpaired Wilcoxon’s test. Box plots show the median (center line), the interquartile range (box, 25th–75th percentiles), and whiskers indicating the minimum and maximum values. Venn diagrams showing the overlap between gene transcripts with increased stability upon EZH2 deficiency and decreased stability upon ADAR1 deficiency (c), or between gene transcripts with decreased stability upon EZH2 deficiency and increased stability upon ADAR1 deficiency (d). P values were calculated by one-tailed Fisher’s exact test. e The selected 3810 gene set (described in c) was subjected to Elsevier Pathway Collection enrichment analysis. f The mRNA decay rate of the selected oncogenes was measured by RT-qPCR analysis using samples collected at various time-points after ActD treatment of control, EZH2-deficient or ADAR1-deficient C4-2 cells. Data represent the mean ± SD from n = 3 biologically independent experiments. g Western blot to detect the protein levels of the selected oncogenes upon EZH2 or ADAR1 knockdown in C4-2 cells. h, i RIP-qPCR assay to monitor the binding of selected oncogenic transcripts to STAU1 upon EZH2 knockdown or EZH2/ADAR1 double knockdown in C4-2 cells. GAPDH mRNA containing no dsRNA structure was served as negative control. Data represent the mean ± SD from n = 3 biologically independent experiments. The protein level of STAU1 in each group was presented in (i). Statistical significance was assessed using two-sided student’s t-test unless otherwise stated. Source data are provided as a Source Data file.