E-GEOD-46821
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA202403
PROVIDER: E-GEOD-46821 | ExpressionAtlas | 2015-07-13
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-46821-analysis-methods.tsv | Tabular | |||
| E-GEOD-46821-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-46821-configuration.xml | Xml | |||
| E-GEOD-46821-percentile-ranks.tsv | Tabular | |||
| E-GEOD-46821.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 53 |
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Project description:Prdm5 suppresses ApcMin-driven intestinal adenomas and regulates monoacylglycerol lipase expression
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Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas
2014-10-31 | E-GEOD-59283 | biostudies-arrayexpress
Project description:We have generated a mouse model for tumor initiation carrying a mutation in APC and lacking IKKα in intestinal epithelial cells. IKKα-deficient intestinal cells primarily failed to generate adenomas, and the few adenomas arising in this background displayed a significant reduction in cell proliferation. Using an in vitro model for intestinal tumoroids (derived from adenoma initiating cells), we have performed RNA sequencing of wild type and IKKα-deficient intestinal tumoroids. This has demonstrated that epithelial IKKα controls transcription of stem cell-related genes and genes associated with proliferation and apoptosis.
2018-04-17 | GSE101415 | GEO
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
Project description:To address the in vivo relevance of CSF1R regulation by miR-34a during intestinal tumor formation, we generated ApcMin/+ mice with intestinal-epithelial cell (IEC)-specific deletions of the Mir34a and/or Csf1r genes. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a and/or Csf1r were compared.
2022-10-04 | GSE167448 | GEO
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.
2011-04-19 | GSE21392 | GEO
Project description:Background and aims: The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers. Methods: We investigated the role of Stat3 in intestinal tumors using mice with conditional ablation of Stat3 in intestinal epithelial cells (Stat3deltaIEC). Results: In the APCmin mouse model of intestinal cancer, genetic ablation of Stat3 reduced the multiplicity of early adenomas. However, loss of Stat3 promoted tumor progression at later stages leading to formation of invasive carcinomas which significantly shortened the lifespan of Stat3deltaIEC APCmin/+ mice. Interestingly, loss of Stat3 in tumors of APCmin/+ mice had no significant impact on cell survival and angiogenesis but promoted cell proliferation. A genome-wide expression analysis of Stat3-deficient tumors suggested that Stat3 negatively regulates intestinal cancer progression via the cell adhesion molecule Ceacam1. Conclusions: Our data suggest that Stat3 impairs progression of intestinal tumors. Therefore, detrimental effects on tumor progression have to be considered upon therapeutic targeting of the Stat3 signaling pathway in intestinal cancer.
2009-12-01 | GSE17841 | GEO
Project description:Leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) is a pan-ErbB negative regulator and intestinal stem cell marker downregulated in many malignancies. Over 91% Lrig1-CreERT2/CreERT2 (Lrig1-/-) mice developed duodenal adenomas, providing the first in vivo evidence Lrig1 acts as a tumor suppressor. We thus characterize the differential expressing transcripts in these duodenal adenomas to explore the pathegenesis. Elevated expression of the Egfr ligands was detected in adenomas compared to adjacent normal tissue. These adenomas also expressed the gastric-specific genes Gastrokine1 and Mucin5ac, indicating gastric metaplasia. In this dataset, we include the expression data obtained from proximal adenomas as well as adjacent normal tissue and wildtype proximal duodenum. These data are used to obtain 679 upregulated and 874 downregulated transcripts in tumors.
2015-01-04 | GSE64640 | GEO
Project description:Small intestinal adenomas in mice with Apc deficiency following tamoxifen-induced genetic recombination.
2021-02-19 | GSE167008 | GEO
Project description:Constitutive activation of the Wnt pathway leads to adenoma formation, an obligatory step towards intestinal cancer. In view of the established role of Wnt in regulating stemness, we attempted the isolation of cancer stem cells (CSCs) from Apc- and Apc/KRAS-mutant intestinal tumours. Whereas CSCs are present in malignant Apc/KRAS–mutant carcinomas, they appear to be very rare (<10-6) in the benign Apc–mutant adenomas. In contrast, the Lin-CD24hiCD29+ subpopulation of adenocarcinoma cells appear to be enriched in CSCs with increased levels of active -catenin. Expression profiling analysis of the CSC-enriched subpopulation confirmed their enhanced Wnt activity and revealed additional differential expression of other signalling pathways, growth factor binding proteins, and extracellular matrix components. As expected, genes characteristic of the Paneth cell lineage (e.g. defensins) are co-expressed together with stem cell genes (e.g. Lgr5) within the CSC-enriched subpopulation. This is of interest as it may indicate a cancer stem cell niche role for tumor-derived Paneth-like cells, similar to their role in supporting Lgr5+ stem cells in the normal intestinal crypt. Overall, our results indicate that oncogenic KRAS activation in Apc-driven tumours results in the expansion of the CSCs compartment by increasing b-catenin intracellular stabilization. To identify molecular differences between stem-like and more differentiated (bulk) tumour cells from Apc1638N/+ and Apc1638N/+/KRASV12G intestinal adenomas and adenocarcinomas, we isolated total RNA from 104 Lin-CD24hiCD29+, Lin-CD24medCD29+/Lin-CD24loCD29+ and Lin- (bulk) tumour cells from 5 individual mice of each genotype (Apc1638N/+ and Apc1638N/+/KRASV12G). Total RNA samples were then employed to hybridize oligonucleotide microarrays (Affymetrix Mouse Genome 430A 2.0 Array) according to conventional protocols.
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