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Crypt density and recruited enhancers underlie intestinal tumour initiation

ABSTRACT: Crypt density and recruited enhancers underlie intestinal tumour initiation

PROVIDER: PRJNA1007859 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25722165.fastq.gz	Fastqsanger.gz
	SRR25722166.fastq.gz	Fastqsanger.gz
	SRR25722167.fastq.gz	Fastqsanger.gz
	SRR25722168_1.fastq.gz	Fastqsanger.gz
	SRR25722168_2.fastq.gz	Fastqsanger.gz

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Crypt density and recruited enhancers underlie intestinal tumour initiation

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Crypt density and recruited enhancers underlie intestinal tumour initiation

Project description:Oncogenic mutations that drive colorectal cancer can be present in healthy intestines for long periods without overt consequence. Mutation of Adenomatous polyposis coli (Apc), the most common initiating event in conventional adenomas, activates Wnt signaling, hence conferring fitness on mutant intestinal stem cells (ISCs). Apc mutations may occur in ISCs that arose by routine self-renewal or by dedifferentiation of their progeny. Although ISCs of these different origins are fundamentally similar, it is unclear if both generate tumours equally well in uninjured intestines. Also unknown is whether cis-regulatory elements are substantively modulated upon Wnt hyperactivation or as a feature of subsequent tumours. Here, we show in two mouse models that adenomas are not an obligatory outcome of Apc deletion in either ISC source but require proximity of mutant intestinal crypts. Reduced crypt density abrogates, and aggregation of mutant colonic crypts augments, adenoma formation. Moreover, adenoma-resident ISCs open chromatin at thousands of enhancers that are inaccessible in Apc-null ISCs not associated with adenomas. These cis-elements explain adenoma-selective gene activity and persist, with little further expansion of the repertoire, as other oncogenic mutations accumulate. Thus, cooperativity between neighbouring mutant crypts and new accessibility at specific enhancers are key steps early in intestinal tumourigenesis.

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Crypt density and recruited enhancers underlie intestinal tumour initiation

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Crypt density and recruited enhancers underlie intestinal tumour initiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-11-15 | GSE241384 | GEO

Spatial tissue proteomics analysis of laser capture microdisscted intestinal crypt compartment

Project description:Crypt hyperplasia is a key feature of celiac disease and various other small intestinal inflammatory conditions. By undertaking mass spectrometry-based tissue proteomics of the gut epithelial crypt zone, we found that active celiac disease is characterized by a strong interferon-γ (IFN-γ) signal. This signal, hallmarked by increased expression of MHC molecules, coincides with a markedly reduced expression of proteins associated with fatty acid metabolism. We observed similar crypt hyperplasia and proteomic alterations in wild-type mice treated with IFN-γ, but not in mice that lack the IFN-γ receptor in gut epithelial cells. IFN-γ is thus a driver of crypt hyperplasia in celiac disease by acting directly on crypt epithelial cells. This dataset contains proteomics analysis of crypt compartment samples isolated by laser capture microdissection small intestinal crypt compartment from C57/Bl6 mice injected i.p. with 0-1-2-4-6 or 9 doses interferon gamma every 8 hour.

2025-08-08 | PXD062684 | Pride

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