Fig. 1

Global regulators of poly(A) site selection correlate with 3′ UTR length in all cancer subtypes except colorectal adenocarcinoma. A Graphical summary of poly(A) site modulators and how they are purported to act globally based on computational correlations with 3′ UTR measurements and targeted knockdown experiments. B Workflow to assess global correlations of gene expression and a summary statistic of 3′ UTR length. For each sample, the 3′ UTR length is calculated per gene using previously published measurements using DaPars [11] for all TCGA data. For each sample, a summary statistic of 3′ UTR length was calculated by taking the median of all imputed 3′ UTR lengths, referred to as median 3′ UTR. We then quantify gene expression (transcripts per million, TPM) for all coding genes per RNA-seq sample across the TCGA RNA-seq datasets. Then for each gene a Pearson correlation was completed comparing median 3′ UTR length and gene expression per gene, per dataset. C Scatter plot of 3′ UTR length and PABPN1 expression (TPM) for four TCGA datasets. Each point represents a single RNA-seq sample. R and p value reflective of the Pearson correlation. D Scatter plot of 3′ UTR length and CSTF2T expression (TPM) for four TCGA datasets. Each point represents a single RNA-seq sample. R and p value reflective of the Pearson correlation. E Correlation matrix of all 30 datasets comparing calculated Pearson correlation coefficients comparing gene expression of each individual gene versus median 3′ UTR. Pairwise dataset correlations were calculated using Pearson correlation. F Violin plot of the median pairwise Pearson correlation comparing all analyzed gene expression—3′ UTR correlations obtained for each cohort to one another