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E-MTAB-4007

ABSTRACT: Transcription profiling of colonic mucosa of Apc Min/+ mice fed with maslinic acid (MA) to study the underlying mechanisms by which MA inhibits intestinal tumorigenesis

OTHER RELATED OMICS DATASETS IN: MTBLS240

PROVIDER: E-MTAB-4007 | ExpressionAtlas | 2015-11-02

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-4007-analysis-methods.tsv	Tabular
	E-MTAB-4007-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-4007-configuration.xml	Xml
	E-MTAB-4007-percentile-ranks.tsv	Tabular
	E-MTAB-4007.condensed-sdrf.tsv	Tabular

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Genome-wide analysis of gene expression in partial Dnmt3a deleted colon mucosa cells of APC(Min/+) mice

Project description:Analysis of gene expression in partial Dnmt3a deleted colon mucosa cells of APC(Min/+) mice. In the present study the influence of Dnmt3a deletion on colonic tumorigenesis, gene expression and DNA methylation was analyzed. Results provide important information about the role of Dnmt3a in colonic tumorigenesis.

2015-06-01 | GSE48115 | GEO

Maslinic acid-enriched diet decreases intestinal tumorigenesis in Apc(Min/+) mice through transcriptomic and metabolomic reprogramming

Project description:Chemoprevention is a pragmatic approach to reduce the risk of colorectal cancer, one of the leading causes of cancer-related death in western countries. In this regard, maslinic acid (MA), a pentacyclic triterpene extracted from wax-like coatings of olives, is known to inhibit proliferation and induce apoptosis in colon cancer cell lines without affecting normal intestinal cells. The present study evaluated the chemopreventive efficacy and associated mechanisms of maslinic acid treatment on spontaneous intestinal tumorigenesis in Apc(Min/+) mice. Twenty-two mice were randomized into 2 groups: control group and MA group, fed with a maslinic acid-supplemented diet for six weeks. MA treatment reduced total intestinal polyp formation by 45% (P<0.01). Putative molecular mechanisms associated with suppressing intestinal polyposis in Apc(Min/+) mice were investigated by comparing microarray expression profiles of MA-treated and control mice and by analyzing the serum metabolic profile using NMR techniques. The different expression phenotype induced by MA suggested that it exerts its chemopreventive action mainly by inhibiting cell-survival signaling and inflammation. These changes eventually induce G1-phase cell cycle arrest and apoptosis. Moreover, the metabolic changes induced by MA treatment were associated with a protective profile against intestinal tumorigenesis. These results show the efficacy and underlying mechanisms of MA against intestinal tumor development in the Apc(Min/+) mice model, suggesting its chemopreventive potential against colorectal cancer.

2017-02-09 | MTBLS240 | MetaboLights

E-GEOD-55356

Project description:p38a-dependent gene expression in the colonic mucosa

2014-07-09 | E-GEOD-55356 | ExpressionAtlas

Quantitative proteomics of intestinal mucosa from male mice lacking intestinal epithelial insulin receptors

Project description:The goal of the present study was to determine whether loss of the insulin receptor alters the molecular landscape of the intestinal mucosa, using intestinal-epithelial insulin receptor knockout (IE-irKO) mice and both genetic (IRfl/fl and Villin-cre) controls. Quantitative proteomic analysis by Liquid Chromatography Mass Spectrometry (LC-MS) was deployed on jejunal and colonic mucosa from mice fed a chow- or Western diet (WD). Jejunal mucosa from IE-irKO mice demonstrated alterations in all intestinal cell linages, Paneth, goblet, absorptive and enteroendocrine cells, whereas only goblet and absorptive cells were affected in the colon. There was also a significant effect of the WD on the gut proteome. A significant reduction was detected in Paneth cell proteins with anti-microbial activity, including lysozyme C-1, angiogenin-4, cryptdin-related sequence1C-3 and -2, a-defensin 17 and intelectin-1a. The key protein expressed by goblet cells, mucin-2, was also reduced in the IE-irKO mice. Proteins involved in lipid metabolism, including aldose reductase-related protein 1, 15-hydroxyprostaglandin dehydrogenase [NAD(+)], apolipoprotein A-II and pyruvate dehydrogenase kinase isozyme 4, were increased in the mucosa of WD-fed IE-irKO mice as compared to controls. In contrast, expression of the nutrient-responsive gut hormones, glucose-dependent insulinotropic polypeptide and neurotensin, was reduced in the jejunal mucosa of IE-irKO mice, and there was a reduction in proteins of the P-type ATPases and the solute carrier-transporter family in the colon of WD-fed IE-irKO mice. In conclusion, IE-irKO mice display a distinct molecular phenotype, suggesting a biological role of insulin and its receptor in determining differentiated cell-specificity in the intestinal epithelium.

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Non-tumor/tumor intestinal tissue of control or intestine-specific HAI-1 deficient Apc(Min/+) mice

Project description:To analyse roles of HAI-1/Spint1 in intestinal tumorigenesis, we examined the effect of intestine-specific deletion of Spint1 gene on Apc(Min/+) mice. The loss of Hai-1/Spint1 significantly accelerated tumor formation in ApcMin/+ mice and shortened their survival periods. Mouse small intestine tumor tissue or background mucosa lacking macroscopically visible tumors were proceeded to RNA extraction and hybridization on microarrays (Affymetrix Mouse Genome 430 2.0 Array). Non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox) mice and non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox)/Vil-Cre mice were analysed. The experiment was repeated respectively.

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Increased tumourigenesis in ApcMin/+ mice fed with a Western-type diet associates with changes in PDK4, Erk/Akt and mTor pathways, intestinal immunity and the expression of energy metabolism-related genes

Project description:Western diet enhances intestinal tumorigenesis in Min/+ mice, associating with mucosal metabolic and inflammatory stress and loss of Apc heterozygosity We investigated the interaction of WD and heterozygous mutation in the Apc gene in the histologically normal intestinal mucosa of ApcMin/+ (Min/+) mice. AIN-93G diet vs. a diet modified from AIN-93G, with high fat and low fiber, vitamin D, calcium and folate. (66.4% of total fat from milk, and 33.6% from rapeseed and sunflower oil)

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p38a-dependent gene expression in the colonic mucosa

Project description:Gene expression in the colonic mucosa of wild-type and p38a-knockout intestinal epithelial cells (IECs) were compared. C57BL/6 wild-type mice, and intestinal epithelial cell-specific p38a-knockout mice on a C57BL/6 background were used for isolation of colonic mucosa

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p38a-dependent gene expression in the colonic mucosa

2014-07-01 | E-GEOD-55356 | biostudies-arrayexpress

Transcription profiling by array of colonic epithelial cells from mice starved, subsequently refed with or without antibiotics metronidazol and vancomycin

Project description:Oral food intake maintains gastrointestinal cell turnover and impacts the morphology and function of intestinal epithelial cells. However, the underlying mechanism is not fully elucidated, especially in the large intestine. Therefore, we analyzed the colonic epithelial cell turnover in starved and re-fed mice. EpCAM+CD45- colonic epithelial cells (ECs) in re-fed mice treated with or without antibiotics were isolated and sorted by FACS for RNA extraction and hybridization on Affymetrix microarrays.

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E-GEOD-59071

Project description:Microarray analysis of colonic mucosa biopsies in patients with inflammatory bowel disease

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