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Neu5Gc intake increases the expression of colorectal cancer-related genes in the APCMin+ mouse

ABSTRACT: Neu5Gc intake increases the expression of colorectal cancer-related genes in the APCMin+ mouse

PROVIDER: PRJNA902357 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22312900_1.fastq.gz	Fastqsanger.gz
	SRR22312900_2.fastq.gz	Fastqsanger.gz
	SRR22312885_1.fastq.gz	Fastqsanger.gz
	SRR22312885_2.fastq.gz	Fastqsanger.gz
	SRR22312886_1.fastq.gz	Fastqsanger.gz

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Neu5Gc intake increases the expression of colorectal cancer-related genes in the APCMin+ mouse

Project description:Clinical cohort data suggest that high consumption of red meat containing N-glycolylneuraminic acid (Neu5Gc) may increase colorectal prevalence, therefore, we investigated the effect of high Neu5Gc intake on colon cancer using the APCMin/+ mouse model . Ten APCMin/+ male mice were divided into two groups and fed normal (control group: 0.0507 mg per mouse per day) and high concentrations (treatment group: 1.014 mg per mouse per day) of Neu5Gc to mimic Normal and excessive consumption of red meat in humans, respectively. After two weeks of feeding, colorectal and liver were collected for histopathological diagnosis and transcriptome analysis.

2023-11-30 | GSE218116 | GEO

Intestinal tumor expression data from Apcmin/+ mice gavaged by feces from healthy controls or colorectal cancer patients

Project description:Colorectal cancer (CRC) is closely related to gut dysbiosis. We investigated the effects of imbalanced gut microbiota on the progression of intestinal adenoma in Apcmin/+ mice model using fecal microbiota transplantation (FMT). Administration of feces from CRC patients increased tumor proliferation and decreased apoptosis in tumor cells. Abnormal expression of genes related to Wnt-protein binding and lipid metabolic process was observed.

2019-09-16 | GSE136682 | GEO

Effects of Wumei Wan (WMW) on Colorectal Protein Expression in APCmin/+ Mice

Project description:Eight-week-old C57BL/6 or APCmin/+ mice were fed a high-fat diet ad libitum and randomly divided into four groups:(1)Control group (wild-type C57BL/6 mice), (2)Model group (APCmin/+ mice), (3)WMW-treated group (APCmin/+ mice receiving Wumei Pill at 17 g/kg/day via oral gavage), and (4)BBR group (APCmin/+ mice administered berberine at 100 mg/kg/day via oral gavage) Following the 10-week intervention, colorectal tissues were collected and subjected to 4D label-free quantitative proteomics analysis to investigate the regulatory effects of WMW on protein expression profiles in APCmin/+ mice.

2025-06-12 | PXD064966 |

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

Inhibiting neutrophils activation by long-term administration of 5-amino salicylic acid reduces colitis-associated colorectal tumor burden in ApcMin/+ mice

Project description:Objective The risk of ulcerative colitis (UC)-associated colorectal cancer (CRC) increases with the duration of UC. Oral 5-aminosalicylic acid (5-ASA) formulations are the first-line treatment for mild-to-moderate UC; nevertheless, preventive effect of oral 5-aminosalicylic acid (5-ASA) formulations on UC-associated CRC remains unsolved. We investigated the impact of 5-ASA to colitis-associated neoplasia in C57BL/6J-ApcMin heterozygous (ApcMin/+) mice. Design ApcMin/+ mice exposed to 1.5 w/v% dextran sulfate sodium (DSS) ad libitum for 3 days followed by 25 days of tap water to develop colitis-associated neoplasia. Mice were intracolorectally administrated with 5-ASA to evaluate the effects on the number of tumors. The mechanism of action was presumed by microarray analysis using in vivo samples and was confirmed by in vitro culture of HT-29, a human colorectal adenocarcinoma cell line with supernatant of human primary neutrophils. Results A remission between acute and recurrent episodes of diarrhea, which were ameliorated by 5-ASA treatment were observed in this model. The number of tumors was reduced by continuous 5-ASA administration in this model. This reduction was abolished by withdrawal of 5-ASA in remission period compared to continuous 5-ASA administration. Microarray analysis revealed that neutrophils were involved in the protective mechanism of 5-ASA against proliferation of tumors. Additionally, calprotectin production from human primary neutrophil as activation marker was strongly correlated with proliferation of HT-29.

2019-06-26 | GSE83749 | GEO

Expression data from cav1-/+apcmin/+ mouse intestinal tissue

Project description:We used microarrays to decipher the global programme of gene expression in normal colon tissue versus colorectal tumor tissue explants from 6 months old cav1-/+ apcmin/+ mice and identified distinct classes of differentially regulated genes.

2019-01-10 | GSE124838 | GEO

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

Notch signaling suppresses the progression of colorectal tumorigenesis

Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.

2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress

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