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Murine small intestinal crypt cells: IGF-1 stimulated vs. control

ABSTRACT: microRNA profiling of mouse small intestinal crypt cells comparing control untreated with cells treated with insulin growth factor-1 (IGF-1). IGF-1 stimulated cell proliferation, as observed in Brdu incoporation assay.

ORGANISM(S): Human gammaherpesvirus 8 Rattus norvegicus Mus musculus JC polyomavirus Betapolyomavirus macacae Murid gammaherpesvirus 4 Homo sapiens Human immunodeficiency virus 1 Human betaherpesvirus 5 Betapolyomavirus hominis Human alphaherpesvirus 1 human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE20133 | GEO | 2010/11/01

SECONDARY ACCESSION(S): PRJNA125663

REPOSITORIES: GEO

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Murine small intestinal crypt cells: IGF-1 stimulated vs. control

Project description:microRNA profiling of mouse small intestinal crypt cells comparing control untreated with cells treated with insulin growth factor-1 (IGF-1). IGF-1 stimulated cell proliferation, as observed in Brdu incoporation assay. Two condition experiment. Control vs IGF-1 treatment. Biological replicates: 3 control, 3 treated. Independently grown and harvested. One replicate per array

2010-11-01 | E-GEOD-20133 | biostudies-arrayexpress

Murine small intestinal crypt cell line IEC-6: control vs. TGF-beta stimulated

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Murine small intestinal crypt cell line IEC-6: control vs. TGF-beta stimulated

Project description:microRNA profiling of rat small intestinal crypt cell IEC-6. Comparing control untreated with cells treated with transforming growth factor-beta (TGF-beta). TGF-beta stimulated cell differentiation, as observed in the stimulation of intestinal epithelial cell markers (alkaline phophotase, villin, aminopeptidase N, etc.). Two condition experiment. Control vs TGF-beta treatment. Biological replicates: 3 control, 3 treated. Independently grown and harvested. One replicate per array

2012-06-18 | E-GEOD-20982 | biostudies-arrayexpress

Mammary Tissue: Wild type mammary glands vs IGF-IR induced mammary tumors vs IGF-IR independent tumors

Project description:Molecular profiling was used to classify mammary tumors that develop in MTB-IGFIR transgenic mice. It was determined that the primary mammary tumors (PMT), which develop due to elevated expression of the type I insulin-like growth factor receptor (IGF-IR) in mammary epithelial cells, most closely resemble murine tumors with basal-like or mixed gene expression profiles and with human basal-like breast cancers. Downregulation of IGF-IR transgene in MTB-IGFIR tumor-bearing mice leads to the regression of most of the tumors followed by tumor re-appearance in some of the mice. These tumors that re-appear following IGF-IR transgene downregulation do not express the IGF-IR transgene and cluster with murine mammary tumors that express a mesenchymal gene expression profile and with human claudin-low breast cancers. Therefore, IGF-IR overexpression in murine mammary epithelial cells induces mammary tumors with primarily basal-like characteristics while tumors that develop following IGF-IR downregulation express a gene signature that most closely resembles human claudin-low breast tumors.

2011-10-01 | GSE32152 | GEO

IGF-1 stimulated C2 skeletal myotube phosphoproteome

Project description:Skeletal muscle is known to adapt dynamically to changes in workload by regulatory processes of the phosphatidylinositide 3-kinase (PI3K)/Akt pathway. We performed a global quantitative phosphoproteomics analysis of contracting mouse C2 myotubes treated with insulin growth factor 1 (IGF-1) as control and additionally MK-2206 or LY294002 to inhibit PI3K/Akt signaling, respectively.

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Intestinal crypt stem and transit cell proliferation and villus cell migration in mice lacking Klf9

Project description:Krüppel-like factor 9 (Klf9), a zinc-finger transcription factor, is implicated in the control of cell proliferation, cell differentiation and cell fate in brain and uterus. Using Klf9 null mutant mice, we have investigated the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination. We report the predominant expression of Klf9 gene in small intestine smooth muscle (muscularis externa). Jejunums null for Klf9 have shorter villi, reduced crypt stem/transit cell proliferation, and altered lineage determination as indicated by decreased and increased numbers of Goblet and Paneth cells, respectively. A stimulatory role for Klf9 in villus cell migration was demonstrated by BrdU labeling. Results suggest that Klf9 controls the elaboration, from small intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination, and of villus cell migration. Keywords: Genetic modification

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Expression data from MCF-7 cells stimulated by Estrogen or IGF-I

Project description:Although estrogen receptor (ER) and insulin-like growth factor (IGF) signaling are important for normal mammary development and breast cancer, cross-talk between these pathways, particularly at the level of gene transcription, remains poorly understood. We performed microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr. IGF-I regulated mRNA of 5-10-fold more genes than estradiol, and many genes were co-regulated by both ligands. Importantly, expression of these co-regulated genes correlated with poor prognosis of human breast cancer. Closer examination revealed enrichment of repressed transcripts. Interestingly, a number of potential tumor suppressors were down-regulated by IGF-I and estradiol. In fact, BLNK, one of the top repressed genes, is a potential growth suppressor in breast cancer cells. Analysis of three down-regulated genes showed that E2-mediated repression occurred independently of IGF-IR, and IGF-I-mediated repression occurred independently of ER. However, repression by IGF-I or estradiol required common downstream kinases. In conclusion, E2 and IGF-I co-regulate a set of genes that affect breast cancer outcome. There is enrichment of repressed transcripts, and the down-regulation is independent at the receptor level. This may be important clinically, as tumors with active ER and IGF-IR signaling may require co-targeting of both pathways. KEYWORDS: multiple group comparison

2011-05-09 | GSE26834 | GEO

Mammary Tissue: Wild type mammary glands vs IGF-IR induced mammary tumors vs IGF-IR independent tumors

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Expression data from MCF-7 cells stimulated by Estrogen or IGF-I

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Gene expression profiling of IR-/-, IGF-1R-/- (dKO) newborn epidermis.

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2013-05-18 | GSE47065 | GEO

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