Skip to main content
Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: CPSF6 links alternative polyadenylation to metabolism adaption in hepatocellular carcinoma progression

Fig. 4

Characteristics of 3 T-seq data. a, b Genomic locations of qualified 3 T-seq reads mapped to the reference genome. c, d Genomic distribution of the poly(A) sites. e, f The statistics of genes with various number of detected poly(A) sites. g, h Scatterplot of CULI for measuring the 3′UTR alteration in CPSF6-overexpressing or CPSF6 knockdown cells when compared with the corresponding control cells (false discovery rate (FDR) = 0.05). i CPSF6-modulated 7 candidate genes. These genes had the shortened 3′UTR in CPSF6-overexpressing HL-7702 cells and the lengthened 3′UTR in CPSF6 knockdown Huh-7 cells. j CPSF6-induced APA shift of NQO1. Left, Integrative Genomics Viewer (IGV) genome browser exhibited the poly(A) site usage of NQO1 3′UTR. Right, histogram showed the relative expression of the isoform with distal polyadenylation site (dPAS) relative to the one with proximal PAS (pPAS). k, l The protein levels of NQO1 in the CPSF6-overexpressing HL-7702 cells (k) and the CPSF6 knockdown Huh-7 cells (l) were assessed by western blotting. β-actin was used as internal control

Back to article page