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Deletion of TNF in Winnie-ApcMin/+ mice reveals its dual role in the onset and progression of colitis-associated colorectal cancer

ABSTRACT: Deletion of TNF in Winnie-ApcMin/+ mice reveals its dual role in the onset and progression of colitis-associated colorectal cancer

PROVIDER: PRJEB57223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10451772_1.fastq.gz	Fastqsanger.gz
	ERR10451772_2.fastq.gz	Fastqsanger.gz
	ERR10451773_1.fastq.gz	Fastqsanger.gz
	ERR10451773_2.fastq.gz	Fastqsanger.gz
	ERR10451774_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Deletion of TNF in Winnie-ApcMin/+ mice reveals its dual role in the onset and progression of colitis-associated colorectal cancer

Project description:Colorectal cancer (CRC) is among the best examples depicting the relationship between inflammation and increased cancer risk. The introduction of new therapeutic options targeting the inflammatory mediators has been shown to markedly decrease the overall risk of CRC even though their chemopreventive potential is still under debate [1,2]. Specifically, conflicting reports exist concerning the relationship between Infliximab, a monoclonal antibody that specifically blocks Tumor Necrosis Factor (TNF), and an increased risk of CRC in patients with Inflammatory Bowel Disease (IBD). To address the axis between TNF and CRC development and progression, we depleted the Tnf from our previously established murine model of colitis-associated cancer (CAC), the Winnie-ApcMin/+ line. Surprisingly, a detailed histological characterization, demonstrated that the deletion of Tnf in Winnie-ApcMin/+ mice resulted in an initial reduction of dysplastic lesions incidence in 5-week-old mice, followed by faster disease progression with a unique molecular pattern at 8 weeks. Our results highlight that TNF could exert a dual role in CAC supporting the promotion of neoplastic lesions onset at the early stage of the disease and inducing their reduction during disease progression.

2023-05-01 | E-MTAB-12356 | biostudies-arrayexpress

Deletion of TNF in Winnie-ApcMin/+ mice reveals its protective role in the progression of colorectal cancer

Project description:To examine the effects of chronic, low-grade inflammation on the pathogenesis of colorectal cancer (CRC), we developed a novel murine model of colitis-associated cancer by crossing Winnie mice with ApcMin/+ mice thus combining the inflammatory background with a genetic predisposition to develop small intestinal polyposis, respectively. Winnie-ApcMin/+ mice showed early, spontaneous occurrence of colonic dysplastic lesions with a distinct molecular signature. Since TNF is a major clinical target for suppression of chronic intestinal inflammation, we investigated its impact on Winnie-ApcMin/+ model. Surprisingly, deletion of Tnf in Winnie-ApcMin/+ mice resulted in an initial reduction of dysplastic lesions at disease onset, but facilitated disease progression with a unique molecular footprint. Our results confirm that even a mild, but chronic, inflammation represents a crucial risk factor in individuals genetically-predisposed to CRC, and support a dual role for TNF in the onset vs. progression towards CRC.

2021-12-31 | GSE138722 | GEO

Deletion of TNF in Winnie-ApcMin/+ mice reveals its protective role in the progression of colorectal cancer

Project description:Deletion of TNF in Winnie-ApcMin/+ mice reveals its protective role in the progression of colorectal cancer

| PRJNA576901 | ENA

Transcriptomic analysis of differentially expressed genes in the Winnie mouse model of chronic colitis

Project description:The Winnie mouse, carrying a missense mutation in the Muc2 gene, is a model for chronic colitis closely resembling the pathological changes of human IBD. Herein, transcriptomic analyses of the differentially expressed genes in the distal colon of Winnie mice with mild colitis and Winnie-Prolapse mice with severe colitis are compared to control C57BL/6 mice. Gene ontology analysis and KEGG pathway analysis demonstrated the upregulation of genes in immune and inflammation-related pathways, metabolic pathways, cancer-related pathways, and neurological processes. Further research into these pathways and individual genes may lead to the identification of new targets for the treatment of IBD. The overexpression of oncogenes, in particular, may serve as an indicator of inflammation progressing to cancer.

2023-10-08 | GSE244558 | GEO

Winnie-APCMin/+ Mice: A Spontaneous Model of Colitis-Associated Colorectal Cancer Combining Genetics and Inflammation.

Project description:(1) Background: Colorectal cancer (CRC) is among the best examples of the relationship between inflammation and increased cancer risk. (2) Methods: To examine the effects of spontaneous low-grade chronic inflammation on the pathogenesis of CRC, we developed a new murine model of colitis-associated cancer (CAC) by crossing Mucin 2 mutated mice (Winnie) with ApcMin/+ mice. (3) Results: The resulting Winnie-ApcMin/+ model combines an inflammatory background with a genetic predisposition to small intestinal polyposis. Winnie-ApcMin/+ mice show an early occurrence of inflammatory signs and dysplastic lesions in the distal colon with a specific molecular signature. (4) Conclusion: The Winnie-ApcMin/+ model is a perfect model to demonstrate that chronic inflammation represents a crucial risk factor for the onset and progression of tumoral lesions in individuals genetically predisposed to CRC.

| S-EPMC7215554 | biostudies-literature

Deletion of TNF in Winnie-<i>APC<sup>Min/+</sup></i> Mice Reveals Its Dual Role in the Onset and Progression of Colitis-Associated Colorectal Cancer.

Project description:Colorectal cancer (CRC) is among the best examples for depicting the relationship between inflammation and cancer. The introduction of new therapeutics targeting inflammatory mediators showed a marked decrease in the overall risk of CRC, although their chemopreventive potential is still debated. Specifically, a monoclonal antibody that blocks tumor necrosis factor (TNF), infliximab, increases CRC risk in inflammatory bowel disease patients. To address the axis between TNF and CRC development and progression, we depleted the Tnf from our previously established murine model of colitis-associated cancer (CAC), the Winnie-ApcMin/+ line. We characterized the new Winnie-APCMin/+-TNF-KO line through macroscopical and microscopical analyses. Surprisingly, the latter demonstrated that the deletion of Tnf in Winnie-ApcMin/+ mice resulted in an initial reduction in dysplastic lesion incidence in 5-week-old mice followed by a faster disease progression at 8 weeks. Histological data were confirmed by the molecular profiling obtained from both the real-time PCR analysis of the whole tissue and the RNA sequencing of the macrodissected tumoral lesions from Winnie-APCMin/+-TNF-KO distal colon at 8 weeks. Our results highlight that TNF could exert a dual role in CAC, supporting the promotion of neoplastic lesions onset in the early stage of the disease while inducing their reduction during disease progression.

| S-EPMC9737576 | biostudies-literature

Cytauxzoon felis strain:Winnie

Project description:Cytauxzoon felis strain:Winnie Genome sequencing and assembly

| PRJNA196611 | ENA

Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

Project description:Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

| PRJNA413950 | ENA

Genome-wide analysis expression of ileum tumor samples from FVBN/APCmin and iPGC-1β/APCmin

Project description:Analysis of metabolic pathway gene expression. The hypothesis tested in the present study is to assess mRNA level changes in metabolic genes in intestinal tumors from APCmin mice overexpressing PGC-1β specifically in the intestine. Total RNA obtained from ileum tumor samples from iPGC-1β/APCmin mice was compared to the total RNA extracted from FVBN/APCmin mice.

2015-03-01 | E-GEOD-61642 | biostudies-arrayexpress

Microarray analysis of ApcMin/+ and D6(ACKR2)-/-ApcMin/+ tumors

Project description:Mast cells have been suggested to either promote or suppress tumor progression but the mechanisms underlying these outcomes are unclear. Here, we show that mice with a heterozygous mutation in the adenomatous polyposis coli gene (ApcMin/+) displayed reduced intestinal tumor burden and increased survival in the background of the chemokine decoy receptor ACKR2 deficiency (ACKR2-/-). The ACKR2-/-ApcMin/+ tumors showed increased infiltration of mast cells. In mast cell-deficient Sash (c-kitW-sh/W-sh) ACKR2-/-ApcMin/+ mice the survival advantage was lost as the tumors grew rapidly and adoptive transfer of mast cells reduced the tumor burden in these mice. The tumor burden is also increased in Rag2-/-ACKR2-/-ApcMin/+ mice and the protection is reconstituted by adoptively transferred CD8+ T-lymphocytes. Mast cells from ACKR2-/- mice expressed elevated levels of chemokine receptors CCR2 and CCR5 and are also efficient in antigen presentation and activation of CD8+ T-cells. Mast cell-derived leukotriene B4 is a critical mediator of CD8+ T-lymphocyte recruitment as the BLT1-/-ACKR2-/-ApcMin/+ mice are highly susceptible to intestinal tumor induced mortality. Taken together, these data demonstrate that chemokine mediated mast cell recruitment is essential for initiating LTB4/BLT1 regulated CD8+ T-cell homing and generation of effective anti-tumor immunity against intestinal tumor development.

2017-12-31 | GSE104829 | GEO

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