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

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

PROVIDER: PRJNA576901 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10258436_1.fastq.gz	Fastqsanger.gz
	SRR10258436_2.fastq.gz	Fastqsanger.gz
	SRR10258437_1.fastq.gz	Fastqsanger.gz
	SRR10258437_2.fastq.gz	Fastqsanger.gz
	SRR10258438_1.fastq.gz	Fastqsanger.gz

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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 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 dual role in the onset and progression of colitis-associated colorectal cancer

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

| PRJEB57223 | ENA

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

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

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

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

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

Genome-wide analysis of gene expression profile of Intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16

Project description:Changes in gene expression profile of intestinal (ILEUM) Tumors from APCmin/+/VP16LXRa vs APCmin/+/VP16. The hypothesis tested in the present study was that LXRa overexpression influence cancer growth modulating lipid metabolism in cancer cells. Results provide the information that LXRa induces genes encoding proteins able to regulate cholesterol efflux. Total RNA obtained from Ileum tumors from APCmin/+/VP16LXRa mice was compared to total RNA extracted from APCmin/+/VP16 mice.

2013-02-05 | E-GEOD-44071 | biostudies-arrayexpress

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