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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE220310 | GEO | 2023/03/28

REPOSITORIES: GEO

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [Hi-C]

Project description:We have previously shown that EPR favors the interaction between Mettl7a1 promoter and a distal enhancer element. To comprehensively map long-range interactions between promoters and distal regulatory elements that are affected by EPR KO in large intestine, we preformed Promoter capture Hi-C experiments. Crypts were purified from proximal colon of two EPR fl/fl control and two EPR cKO mice. Hi-C libraries were constructed and hybridized with biotinylated RNA probes from the Arima mouse promoter panel designed to hybridize the promoters of 25752 mouse genes. Captured libraries were sequenced and bioinformatically analyzed. Our results indicate that EPR knockout leads to a rewiring of a number of promoter-enhancer interactions.

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [RNA-seq]

Project description:The lncRNA EPR (a.k.a BC030870) is highly enriched in the gastrointestinal tract in mice and, more specifically, in the large intestine. We generated conditional EPR knock-out in large intestine e and analyzed genome-wide the gene expression changes by RNA-Seq. Total RNA was extracted from the proximal colon of six control (EPR fl/fl) and six knock-out (EPR cKO) mice. Libraries were constructed and sequenced. Results indicate that EPR knock-out predominantly leads to down-regulation of genes implicated in mucus biogenesis. These results help in explaining the phenotype displayed by EPR cKO mice that is characterized by higher susceptibility to intestinal inflammation and cancer formation.

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

Project description:LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis

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Project description:The long non-coding RNA EPR is expressed in epithelial tissues, binds to chromatin and controls distinct biological activities in mouse mammary gland cells. Because of its high expression in the intestine, in this study we have generated a colon-specific conditional targeted deletion (EPR cKO) to evaluate EPR in vivo functions in mice. EPR cKO mice display epithelium hyperproliferation, impaired mucus production and secretion, as well as inflammatory infiltration in the proximal portion of the large intestine. RNA sequencing analysis reveals a rearrangement of the colon crypt transcriptome with strong reduction of goblet cell-specific factors including those involved in the synthesis, assembly, transport and control of mucus proteins. Further, colon mucosa integrity and permeability are impaired in EPR cKO mice, and this results in higher susceptibility to dextran sodium sulfate (DSS)-induced colitis and tumor formation. Human EPR is down-regulated in human cancer cell lines as well as in human cancers, and overexpression of EPR in a colon cancer cell line results in enhanced expression of pro-apoptotic genes. Mechanistically, we show that EPR directly interacts with select genes involved in mucus metabolism whose expression is reduced in EPR cKO mice and that EPR deletion causes tridimensional chromatin organization changes.

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LncRNA EPR transcriptional activity controls intestinal mucus and prevents susceptibility to inflammation and tumorigenesis [RNA-seq]

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