Tamoxifen-induced Ghr deletion in WT mouse prostates
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PROVIDER: PRJNA811433 | ENA |
REPOSITORIES: ENA
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Project description:Two-month old tamoxifen-inducible Ghr recombination mice (Ghrflox/flox;ROSA26Cre-ERT2+/0) or tamoxifen-control mice (Ghrflox/flox) were treated with 250 mg/kg tamoxifen for five straight days. The dorsolateral prostate of each mouse was collected one month after final treatment and RNA was collected. Samples include
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Project description:Tamoxifen-induced Ghr deletion in SV40 C3(1) T-antigen mouse prostates
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Project description:Seven-month old tamoxifen-inducible Ghr recombination mice in T-antigen mouse model of prostate cancer (Ghrflox/flox;ROSA26Cre-ERT2+/0;SV40 C3(1) T-antigen+/0) or tamoxifen-control mice (Ghrflox/flox;SV40 C3(1) T-antigen+/0) were treated with 250 mg/kg tamoxifen for five straight days. The dorsolateral prostate of each mouse was collected one month after final treatment and RNA was collected. Samples include
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Project description:We employed a quantitative differential proteomics approach to compare the protein expression levels between WT and rss03 deletion mutant (Δrss03), revealing significant differences in some proteins.
2024-03-15 | PXD050638 |
Project description:We used microarrays to detail the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Ptenpc-/- anterior prostates, Ptenpc-/-Smad4pc-/- and Ptenpc-/- anterior prostates, Ptenpc-/-p53pc-/- and Ptenpc-/- anterior prostates at 15 weeks of age. Prostate-specific Pten deletion (Ptenpc-/-) results in prostate intraepithelial neoplasia (PIN) which, following a long latency, can progress to high-grade adenocarcinoma, albeit with minimally invasive and metastatic features. To understand this feeble progression phenotype, we conducted transcriptome comparison of five Ptenpc-/- PIN relative to three wild-type anterior prostate. Moreover, Ptenpc-/-Smad4pc-/- progress to metastasis, while Ptenpc-/-p53pc-/- not progress to metastasis. To understand this phenotype difference, we conducted transcriptome comparison of five Ptenpc-/-Smad4pc-/-to five Ptenpc-/- prostate tumor, and three Ptenpc-/-p53pc-/- to five Ptenpc-/- tumor.
2010-11-05 | E-GEOD-25140 | biostudies-arrayexpress
Project description:We used microarrays to analyze the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Pb-Cre4;PtenLoxP/LoxP anterior prostates, Pb-Cre4;PtenLoxP/LoxP;LrfLoxP/LoxP anterior prostates at 12 weeks of age. Prostate-specific Pten deletion (Pb-Cre4;PtenLoxP/LoxP) results in prostate intraepithelial neoplasia (PIN) which, following a long latency, can progress to high-grade adenocarcinoma, albeit with minimally invasive and metastatic features. However, inactivation of Lrf in the prostate epithelium in combination of Pten results in aggressive prostate tumors. To understand the molecular mechanisms by which loss of Lrf promotes Pten-loss-driven prostate tumorigenesis, we conducted transcriptome comparison of three wild-type anterior prostates, three Pb-Cre4;PtenLoxP/LoxP PIN, and three Pb-Cre4;PtenLoxP/LoxP;LrfLoxP/LoxP anterior prostate tumors.
2013-05-19 | E-GEOD-46473 | biostudies-arrayexpress
Project description:We used microarrays to detail the global gene expression and identified differentially expressed gene list between wild-type anterior prostates and Ptenpc-/- anterior prostates, Ptenpc-/-Smad4pc-/- and Ptenpc-/- anterior prostates, Ptenpc-/-p53pc-/- and Ptenpc-/- anterior prostates at 15 weeks of age.
2010-11-05 | GSE25140 | GEO
Project description:KLF5 is a basic transcription factor that regulates multiple biological processes, but its function in tumorigenesis appears contradictory in the current literature, with some studies showing tumor suppressor activity and others showing tumor promoting activity. In this study, we examined the function of Klf5 in prostatic tumorigenesis using mice with prostate specific deletion of Klf5 and Pten, both of which are frequently deleted in human prostate cancer. Histological and molecular analyses demonstrated that when one Pten allele was deleted, which causes mouse intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth and caused more severe morphological and molecular alterations, and homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Klf5 deletion clearly promoted tumorigenesis in luminal cells, it actually diminished the numbers of Ck5-positive basal cells in the Pten-null tumors. Klf5 deletion also increased the cell proliferation rate in tumors with Pten deletion, which involved extensive activation of the PI3K/AKT and MAPK mitogenic signaling pathways and inactivation of the p15 cell cycle inhibitor. Global gene expression and pathway analyses demonstrated that multiple mechanisms could be responsible for the tumor promoting effect of Klf5 deletion, We used microarrays to detail the global programme of gene expression of Klf5-wildtype and Klf5-null mouse dorsal prostates under Pten-null context to figure out the differential expression profiling underlying tumorigenesis 4 Klf5-wildtype and 4 Klf5-null mouse (6 months age) dorsal prostates under Pten-null context were used for RNA extraction and hybridization on Affymetrix mouse st 1.0 array
2014-06-21 | E-GEOD-58719 | biostudies-arrayexpress
Project description:Tamoxifen-induced deletion of endogenous GlcCer-synthesizing enzyme UDP-glucose:ceramide glucosyltransferase (UGCG) in keratin K14-positive cells results in epidermal GlcCer depletion. We used microarrays to investigate the molecular consequences of Ugcg-depleted mouse epidermis. Ugcgfl/fl K14CreERT2 vs. Ugcgfl/fl samples taken at day 21 post tamoxifen induction
2013-06-12 | E-GEOD-47789 | biostudies-arrayexpress
Project description:A deletion mutation in the growth hormone receptor (GHR) gene results in the inhibition of skeletal muscle growth and fat deposition in dwarf chickens. In this study, microarray techniques were used to detect the miRNA and mRNA expression profiles of 14-day-old embryo and 7-week-old chicken skeletal muscle of deletion-type dwarf chickens and normal-type chickens. Skeletal muscle tissues of Dwarf recessive White Rock chickens and normal recessive White Rock chickens were used to make the microarray assay. Results show the expression of miR-1623 and miR-181b in 14-day-old embryos and of let-7b and miR-128 in 7-week-old chickens. let-7b was the only miRNA found to be completely complementary to its target in the 3'UTR of GHR and inhibited GHR gene expression. KEGG (Kyoto Encyclopaedia of Genes and Genomes) pathway analysis and RT-PCR verified that there were three main signalling pathways regulating the skeletal muscle growth and fat deposition of chickens influenced by the let-7b-regulated GHR gene. The suppression of the cytokine signalling 3 (SOCS3) gene was found to be involved in the signalling pathway of adipocytokines. We found that let-7b is the critical miRNA involved in the regulation of the GHR gene. SOCS3 plays a critical role in the network regulating skeletal muscle growth and fat deposition via let-7b-mediated GHR gene expression.
2012-04-18 | GSE37367 | GEO