E-MTAB-4007
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: MTBLS240
PROVIDER: E-MTAB-4007 | ExpressionAtlas | 2015-11-02
REPOSITORIES: ExpressionAtlas
Dataset's files
| 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 |
Items per page: 5 1 - 5 of 46 |
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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
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
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.
2013-04-01 | E-GEOD-40856 | biostudies-arrayexpress
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)
2017-08-01 | GSE85729 | GEO
Project description:This experiment reports the RNA microarray data from the microarray analysis performed to the RNA isolated from colonic mucosal layer of Apc Min/+ mice. Apc Min/+ mice develop polyps in both the small and large intestine, with a greater incidence of intestinal adenomas observed in the former. We wanted to evaluate if maslinic acid (MA), a natural pentacyclic triterpene widely present in dietary plants and in olive fruit skins, could prevent spontaneous intestinal tumorigenesis in Apc Min/+ mice and through with mechanism MA executes its function. To do so, Apc Min/+ mice were fed for 6 weeks with a standard diet (control animals) or with the same diet supplemented with 100 mg of MA/kg feed (MA-treated animals). After 6 weeks, animals were killed and large intestine of each dead mouse was removed and placed on a plastic plate that was kept at 4ºC. After removal of the rectum, the colon was opened longitudinally with fine scissors, and mucus and feces were washed away. The colonic mucosal layer was incubated in Trizol for 3 min and scraped off of the muscle layer with the edge of a sterile glass slide. Cells were transferred into 800 microL trizol. Total RNA was isolated by using the Trizol method according to the manufacturer's protocol. Subsequently, it was purified by using the RNeasy Mini kit and digesting it with DNase I (Qiagen) according to the manufacturer's protocol. RNA pellets were resuspended in DEPC-treated, RNase-free water, and their purity and quantity were determined spectrophotometrically by using the NanoDrop ND-1000. RNA samples were considered suitable for further processing if their absorbance ratio 260/280 was higher than 1.9. Integrity was tested by using lab-on-a-chip technology on the BioAnalyzer 2100.
2015-10-31 | E-MTAB-4007 | biostudies-arrayexpress
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).
2013-04-01 | GSE40856 | GEO
Project description:Mutation of the adenomatous polyposis coli (APC gene), an early event in the adenoma-carcinoma sequence, is present in 70-80% of sporadic human colorectal adenomas and carcinomas. To test the hypothesis that mutation of the APC gene alters microbial interactions with host intestinal mucosa prior to the development of polyposis, culture-independent methods (targeted qPCR assays and Illumina sequencing of the 16S rRNA gene V1V2 hypervariable region) were used to compare the intestinal microbial composition of 30 six-week old C57BL/6 APCMin/+ and 30 congenic wild type (WT) mice. The results demonstrate that similar to 12-14 week old APCMin/+ mice with intestinal neoplasia, 6 week old APCMin/+ mice with no detectable neoplasia, exhibit an increased relative abundance of Bacteroidetes spp in the colon. Parallel mouse RNA sequence analysis, conducted on a subset of proximal colonic RNA samples (6 APCMin/+, 6 WT) revealed 130 differentially expressed genes (DEGs, fold change ? 2, FDR <0.05). Hierarchical clustering of the DEGs was carried out by using 1-r dissimilarity measurement, where r stands for the Pearson correlation, and Ward minimum variance linkage, in order to reduce the number of input variables. When the cluster centroids (medians) were included along with APC genotype as input variables, analysis of variance and covariance (ANCOVA) with stepwise variable selection, selected two of seven mouse gene clusters, in addition to APC genotype, as significantly associated (p = 0.011 and p = 0.004) with the increased relative abundance of Bacteroidetes spp. One of the two clusters includes several downregulated genes encoding immunoglobulin variable regions and non-protein coding RNAs. These results support the concept that mutation of the APC gene alters colonic-microbial interactions prior to polyposis. It remains to be determined whether interventions directed at ameliorating dysbiosis in APCMin/+mice, such as through probiotics, prebiotics or antibiotics, could reduce tumor formation. Comparing the differential gene expressions in proximal colonic mucosal samples from 6 six-week-old female Apc Min/+ and 6 six-week-old female WT mice
2015-08-24 | E-GEOD-67634 | biostudies-arrayexpress
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.
2017-08-18 | PXD005932 | Pride
Project description:The majority of sporadic colorectal cancer cases are initiated by mutations in the APC tumor suppressor gene leading to constitutive activation of the Wnt/b-catenin signaling pathway and adenoma formation. Several pre-clinical models carrying germline mutations in the endogenous mouse Apc tumor supressor gene have been generated and their phenotype characterized. The predisposition of these mouse models to multiple intestinal adenomas closely resembles the FAP phenotype at the molecular, cellular and phenotypic level and may prove valuable to elucidate the molecular and cellular mechanisms underlying colorectal tumorigenesis. The goal of this study is to establish an expression signature characteristic of intestinal tumors characterized by the inactivation of Apc. Experiment Overall Design: We have compared 3 intestinal tumor samples collected from the mouse model Apc1638N against 2 normal intestinal samples collected from wild type C57Bl6/J animals. In both cases only epithelial cells were used for the signature since we have collected our samples were laser capture microdissected.
2008-06-16 | E-GEOD-9580 | biostudies-arrayexpress
Project description:The majority of sporadic colorectal cancer cases are initiated by mutations in the APC tumor suppressor gene leading to constitutive activation of the Wnt/b-catenin signaling pathway and adenoma formation. Several pre-clinical models carrying germline mutations in the endogenous mouse Apc tumor supressor gene have been generated and their phenotype characterized. The predisposition of these mouse models to multiple intestinal adenomas closely resembles the FAP phenotype at the molecular, cellular and phenotypic level and may prove valuable to elucidate the molecular and cellular mechanisms underlying colorectal tumorigenesis. The goal of this study is to establish an expression signature characteristic of intestinal tumors characterized by the inactivation of Apc. Keywords: Tumor vs Normal intestinal cells
2008-04-01 | GSE9580 | GEO