Fig. 3

A22G at KPC1 transcript is over-edited in iCCA tissues and is mediated by ADAR1-p110. a Vienna prediction of RNA secondary structure of the sequences surrounding the editing site A22G at KPC1 transcript. MFE, minimum free energy. b Editing levels of KPC1 A22G in non-tumor bile duct tissues (NTBD), non-tumor liver tissues (NTL) and iCCA tissues (T) from the patients of VALI1 cohort. Left panel, the representative sequence chromatograms surrounding the editing site A22G at KPC1 transcript. The P value was assessed by paired Student’s t test. c Correlations between the KPC1 A22G editing levels and the mRNA expression levels of ADAR1-p110 or ADAR2, respectively, in iCCA tissues from the patients of VALI1 cohort. The correlations were assessed by Spearman's rank correlation analyses. d and e The sequence chromatograms surrounding the editing site A22G at KPC1 transcript in QBC939 cells upon knockdown of ADAR1 by shRNAs (D) or knockdown of ADAR2 by siRNAs (E). f The sequence chromatograms surrounding the editing site A22G at KPC1 transcript in ADAR1-depleted (by shADAR1-1) QBC939 cells with or without re-expression of ADAR1-p110. g Schematic representation of the editing site A22G (p.M8V) at KPC1 (NCBI No. NM_022064). SPRY, spla/ryanodine receptor domain; RING, really interesting new gene domain; WT, wide-type; EDT, edited