Fig. 6
From: Discovery of physiological and cancer-related regulators of 3′ UTR processing with KAPAC
Analysis of TCGA data sets. a For TCGA data sets with at least five matching normal–tumor pairs with high RNA integrity (mTIN > 70), the distributions of patient-wise medians of tumor–normal tissue differences in average terminal exon lengths are shown. Except for adenocarcinoma of the stomach (STAD), the median is negative for all cancers, indicating global shortening of 3′ UTRs in tumors. b Among 56 matching lung adenocarcinoma (LUAD)-normal tissue pairs (from 51 patients) where global shortening of terminal exons was observed, the CSTF2 expression (in fragments per kilobase per million (FPKM)) was negatively correlated (rP = −0.72, p value = 2.5e-18) with the median of average exon length. c For the same samples as in b, no significant correlation (rP = −0.01, p value = 0.89) between the expression of CSTF2T and the median of average exon length was observed. d Activity profile of the UGUG CSTF2-binding motif inferred from matched LUAD tumor–normal tissue sample pairs (n = 1054). For visibility, ten randomly selected sample pairs are shown instead of all 56. e, f Activity profiles of UUUUU and AUU, the motifs most significantly associated by KAPAC with changes in PAS use in colon adenocarcinoma (COAD; number of PAS n = 1294) (e) and prostate adenocarcinoma (PRAD; number of PAS n = 1835) (f), respectively (11 tumor–normal tissue sample pairs in both studies)