Fig. 2

ADAR1 is frequently amplified in iCCA tissues and confers oncogenic roles in iCCA. a Somatic genomic amplifications of ADAR1 in iCCAs from the patients of DISC cohort (n = 15), a previous study (GSE49666; n = 10) and the TCGA-CHOL cohort (n = 29), respectively. DISC, discovery; TCGA-CHOL, the Cancer Genome Atlas-cholangiocarcinoma. b and c Correlations between the relative copy number of ADAR1 and its mRNA expression levels in iCCA tissues from the patients of DISC (B) and TCGA-CHOL (C) cohorts, which were assessed by Spearman’s rank correlation analyses. d-g Knockdown of ADAR1 significantly reduced QBC939 cells growth which was assessed by CCK-8 assays (D), plate cell colony formation (E), migration (F) and invasion (G). h–k Overexpression of ADAR1-p110 or -p150 isoform significantly promoted QBC939 cells growth (H), plate cell colony formation (I), migration (J) and invasion (K). l Kaplan–Meier analyses showed that higher ADAR1 protein levels predict decreased overall survival (OS) and disease-free survival (DFS) rates of iCCA patients from the VALI2 cohort. ADAR1 protein levels were determined by IHC assays, and the IHC scores > 6 were designated as “high”; whereas the others were “low”. The significance was determined by log-rank test. m and N Univariate (M) and multivariate (N) Cox hazard ratios analyses for OS (Up panel) and DFS (Down panel) rates in iCCA patients from the VALI2 cohort. HR, hazard ratio; CI, confidence interval; AFP, alpha-fetoprotein; PVTT, portal vein tumor thrombus. In (D-K), data are presented as the mean ± standard deviation (s.d.). ^*P < 0.05, ^**P < 0.01 and ^***P < 0.001; assessed by Student’s t test