Expression data from RU486 treated FVB wild-type and MMTV- PAX8PPARg mouse mammary tumors
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33753 | GEO | 2012/04/30
SECONDARY ACCESSION(S): PRJNA148409
REPOSITORIES: GEO
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Project description:To determine if RU-486 would be effective as a chemopreventive agent, microarrays were used to analyse global gene expression changes in wild-type vs. MMTV-PAX8PPARg mice to determine their differential response to RU486 RNA was isolated (RNeasy Mini Kit, Qiagen) from progestin/DMBA induced mammary tumors from wi transgenic and wild-type mice treated with placebo or 2.5mg RU486 60-day release pellets
2012-04-29 | E-GEOD-33753 | biostudies-arrayexpress
Project description:We previously found that the Drosophila FoxA transcription Fork Head (FKH) is necessary for reduced insulin signalling to extend lifespan. We have now identified that increased expression of FKH in neurons alone is sufficient to extend healthy lifespan. We carried out RNA-sequencing in head tissue on controls (daGS>InRDN,GFP-RNAi without RU-486) and reduced insulin signalling with control RNAi (daGS>InRDN,GFP-RNAi with RU486) and reduced insulin signalling with FKH RNAi (daGS>InRDN,FKH-RNAi with RU486). InR-DN stock used: K1409A.
2021-02-03 | E-MTAB-9017 | biostudies-arrayexpress
Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516.
2013-05-31 | GSE34109 | GEO
Project description:The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium. We used microarrays to analyse global gene expression changes in MMTV-PDK1 transgenic mice versus wild-type mice and determine any differential responses to GW501516 treatment.
2011-02-05 | GSE27083 | GEO
Project description:Cancer is considered as a disease of a specific organ, but its effects are felt throughout the body. The systemic effects of cancer can lead to weakness in muscles and heart, which hastens cancer-associated death. miR-486 is a myogenic microRNA and its reduced expression in skeletal muscle is observed in muscular dystrophy. Muscle-specific transgenic expression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues skeletal muscle defects in muscular dystrophy animal models. We had previously demonstrated reduced circulating and skeletal muscle levels of miR-486 in several cancer types and lower miR-486 levels correlated with skeletal muscle defects and functional limitations in mammary tumor models. Therefore, skeletal muscle defects induced by cancer could resemble defects observed in various dystrophies, which could be reversed through skeletal muscle expression of miR-486. We performed functional limitations studies and biochemical analysis of skeletal muscles of MMTV-Neu transgenic mice that mimic HER2+ breast cancer and MMTV-PyMT transgenic mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 transgenic mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu, but not in MMTV-PyMT mice. In MMTV-Neu model, miR-486 reversed several of the cancer-induced changes in skeletal muscle including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of phosphorylation of the pre-mRNA processing factor hnRNPA0 and the splicing factor SRSF10. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss-of-function mutation is associated with congenital muscular dystrophy. Thus, similar to muscular dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden in select cancer types.
2022-05-19 | PXD028554 | Pride
Project description:The role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516. RNA was isolated (RNeasy Mini Kit, Qiagen) from mammary gland tissue of transgenic and wild-type mice maintained on normal rodent chow or 0.005% GW501516
2013-05-31 | E-GEOD-34109 | biostudies-arrayexpress
Project description:The role of PDK1 on mammary tumorigenesis and its interaction with PPARdelta, was assessed. Transgenic mice were generated in which PDK1 was expressed in the mammary epithelium. We used microarrays to analyse global gene expression changes in MMTV-PDK1 transgenic mice versus wild-type mice and determine any differential responses to GW501516 treatment. RNA was isolated (RNeasy Mini Kit, Qiagen) from mammary gland tissue from nulliparious transgenic and wild-type mice maintained on normal rodent chow or a diet supplemented with GW501516 for 1 week.
2011-02-05 | E-GEOD-27083 | biostudies-arrayexpress
Project description:Murine models of mammary cancers have proven to be highly informative on numerous fronts including individual gene causation, microenvironmental analyses, and chemoprevention studies. The MMTV-Neu transgenic model of mammary cancer has proven to be a useful model and has been employed in several prevention studies. However, there are certain practical drawbacks to its use including long tumor latencies and a tendency to develop mutations in the transmembrane domain of Neu (unlike human HER2/Neu overexpressing breast cancers). Here we report modifications that were made in an attempt to optimize this mouse model for chemopreventive screening. First, homozygous MMTV-Neu and homozygous P53 KO mice were crossed to create a MMTV-Neu/P53+/- strain (which more closely approximates the genetic make-up of most HER2+ human patients). Second, to overcome the drawback of long tumor latencies, the mice were treated with DMBA for eight weeks. DMBA treatment greatly decreased the latency of mammary carcinomas in the MMTV-Neu mice although the resulting tumors remained histopathologically similar to those from MMTV-Neu control mice. Next, we examined gene expression in tumors derived from MMTV-Neu, MMTV-Neu/p53+/-, and DMBA treated mice. It was found that the characteristic MMTV-Neu tumor-defined expression pattern was still the most prevalent feature of all the MMTV-Neu tumors despite their being crossed to the p53 null allele, treated with DMBA, or both. However, tumors from the DMBA treated animals exhibited many unique gene expression changes including the high expression of stress response, defense, and inflammation genes. Finally, we demonstrated that the RXR agonists UAB30 and Targretin, both inhibited mammary cancer formation in MMTV-Neu mice, including those treated with DMBA. These results demonstrate the potential utility of this murine model for additional chemoprevention studies.
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Project description:Intracellular progesterone receptor (PR) presents two main isoforms: PR-A and PR-B with different function and regulation. Both isoforms have been identified in astrocytomas, the most common and aggressive primary brain tumors in humans. To investigate the role of PR activity in the regulation of gene expression pattern of U373 cells, we evaluated by microarray analysis the profile of genes regulated by progesterone (10 nM), by a progesterone receptor antagonist (RU486, 10 M-BM-5M) or by both steroids. The human astrocytoma cell line U373 was treated with progesterone; the antagonist, RU-486 or a combination of both drugs.Subsecuently, total RNA was extracted and hybridised on Affymetrix Human Gene 1.0 STs.
2014-09-01 | E-GEOD-59262 | biostudies-arrayexpress
Project description:The study was designed in order to identify genes differentially expressed when glucocorticoid signaling is blocked by a glucocorticoid-receptor antagonist (RU486 – mifepristone) in the context of brain inflammation induced by bacterial lipopolysaccharide (LPS). LPS is only able to cause murine brain damage in our experimental conditions upon RU486 pre-treatment. Hence, the study may reveal potential candidate genes to mediate neuroprotection or neurotoxicity. Due to the factorial design of the experiment, RU486 main-effect could be dissociated from the effects resultant of RU486/inflammation interaction. In addition, brain dissection was conducted to verify the effects in the brain side ipsilateral or contralateral to the site of intracerebral LPS infusion. Keywords: Brain, CNS, LPS, Glucocorticoid, RU486, Mifrespitone, Innate immune response, Inflammation, Affymetrix, Gene profile, Neuroprotection, Neurodegeneration, Factorial design.
2007-03-22 | GSE6509 | GEO