Fig. 5: The PDZK1IP1 super-enhancer is regulated by inflammation.

a ATAC-seq track at the PDZK1IP1 SE in primary CRCs from TCGA (n = 81 independent tumors, merged into one track). b–d TRAP motif analysis at consensus open chromatin regions from the PDZK1IP1 SE in primary CRC, where sequences are compared against all human promoters with a Benjamini-Hochberg correction to generate a P-value. e Hallmarks of Cancer GSEA of RNA-seq expression data from PDZK1IP1-high (top 50% mRNA expression) versus PDZK1IP1-low (bottom 50% mRNA expression) primary CRCs from TCGA (n = 342 independent tumors). f–i Hallmarks of Cancer GSEA enrichment signatures from PDZK1IP1-high (top 50% mRNA expression) versus PDZK1IP1-low (bottom 50% mRNA expression) primary CRCs from TCGA (n = 342 independent tumors). j, k PDZK1IP1 expression levels by immunoblot in cytokine stimulated HT29 cells (10 ng/mL, 16 hours) or HT29 subcutaneous xenografts in nude mice. l H3K27ac ChIP-seq track of the PDZK1IP1 SE (underlined) in unstimulated or TNFα, IFNγ, and IL-6 co-stimulated HT29 cells at 10 ng/mL for 16 hours. Y-axes of all ChIP-seq tracks are scaled to the same range [0-122]. m Hallmarks of Cancer GSEA performed on differentially expressed genes from RNA-seq between HT29 xenograft tumors (n = 3 independent tumors) and HT29 parental cells maintained in culture (n = 3 biological replicates). n, o Immunoblot of PDZK1IP1 levels in HT29 xenografts in the presence of WT or deleted RELA or STAT3. p–s Immunoblot of PDZK1IP1 levels in HT29 cells with the indicated treatment for 16 hours. Source data are provided as a Source Data file. NES normalized enrichment score, FDR false discovery rate.