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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: The A-to-I editing of KPC1 promotes intrahepatic cholangiocarcinoma by attenuating proteasomal processing of NF-κB1 p105 to p50

Fig. 7

ADAR1 promotes iCCA progression, at least partly, through the KPC1 p.M8V editing. a The effects of overexpression of wide-type KPC1 (KPC1-WT) and KPC1 p.M8V editing (KPC1-EDT) on plate colony formation, migration and invasion capacities of the ADAR1-p110-overexpressed QBC939 cells. b-d The effects of overexpression of KPC1-WT or KPC1-EDT on NF-κB response in ADAR1-p110-overexpressed QBC939 cells by NF-κB reporter assays (B), qRT-PCR assays (C) and ChIP-qPCR assays (D). The 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. e The effects of overexpression of KPC1-WT or KPC1-EDT on p105 and p50 proteins levels in QBC939 cells upon overexpression of ADAR1-p110. f The correlation of p105 protein levels with the KPC1 RNA A22G editing levels (Up panel) or ADAR1-p110 protein levels (Down panel) in iCCA tissues from the patients of VALI1 cohort. The correlation efficient and P value were calculated by Spearman’s rank correlation analysis. g The correlation of ADAR1 protein levels with the cytoplasmic p105/p50 protein levels in iCCA tissues from the patients of VALI2 cohort. The correlation efficient and P value were calculated by Spearman’s rank correlation analysis. h Functional model of KPC1 p.M8V editing in the development of iCCA

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