Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from H295R_GRÎ± cells following treatment with dexamethasone or RU486

ABSTRACT: The human glucocorticoid receptor (GRÎ±) is overexpressed at the molecular and protein level in malignant human adrenocortical cancers. A stable cell line model of GRÎ± overexpression was established using the H295R human adrenocortical cancer cell line. The following results were obtained from gene expression profiling of H295R_GRÎ± and H295R_Control (empty vector) cells following treatment with either a GRÎ± agonist (dexamethasone), GRÎ± antagonist (RU486) or vehicle (ethanol) control. H295R_GRÎ± and H295R_Control (empty vector) cells were treated in triplicate for 6 hours with dexamethasone 100 nM, RU486 100 nM or vehicle (ethanol) control.

ORGANISM(S): Homo sapiens

SUBMITTER: Roderick Clifton-Bligh

PROVIDER: E-GEOD-64826 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from H295R_GRα cells following treatment with dexamethasone or RU486

Project description:The human glucocorticoid receptor (GRα) is overexpressed at the molecular and protein level in malignant human adrenocortical cancers. A stable cell line model of GRα overexpression was established using the H295R human adrenocortical cancer cell line. The following results were obtained from gene expression profiling of H295R_GRα and H295R_Control (empty vector) cells following treatment with either a GRα agonist (dexamethasone), GRα antagonist (RU486) or vehicle (ethanol) control.

2015-01-10 | GSE64826 | GEO

FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (mRNA)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate and mifepristone (RU486) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Expression profiling by microarray of LNCaP-1F5 cells treated with vehicle, 100 nM 5a-dihydrotestosterone (DHT), 100 nM dexamethasone (Dex), 1000 nM cyproterone acetate (CPA), 100 nM mifepristone (RU486) and combination of 100 nM DHT,100 nM Dex for 24 hours.

2013-02-05 | E-GEOD-39654 | biostudies-arrayexpress

Tissue-specific alteration of gene expression and function by RU486 and the GeneSwitch system

Project description:The drug-inducible GeneSwitch (GS)-Gal4 transgene expression system is routinely used in Drosophila aging and behavioral studies to avoid the confounding effects related to genetic background mutations. Here, we report transcriptional and functional defects that are induced by RU486 in a stock- and tissue-dependent manner, such as defects in flight and mitochondrial gene expression. Our findings indicate that side effects induced by RU486 need to be considered when interpreting the observed phenotypes, and proper controls, consisting of ethanol-treated GS-Gal4 flies and RU486-induced expression of mock transgenes, should always be included

2019-06-10 | GSE129815 | GEO

Corticosterone regulation of mRNAs and and corresponding RU486 antagonism in astrocytes in vitro

Project description:Analysis of mRNA gene expression changes mediated by natural glucocorticoid ligand corticosterone in mouse cortical primary astrocyte cultures; also, parallel analysis of RU486 (mifepristone) antagonism of corticosterone-mediated mRNA changes. Total RNA obtained from astrocyte cultures subjected to 2, 4, or 6 hours of (1) 100nM corticosterone alone, (2) 500nM RU486 alone, or (3) 100nM corticosterone + 500nM RU486 exposure compared to vehicle control astrocyte cultures.

2013-01-09 | E-GEOD-39270 | biostudies-arrayexpress

Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice

Project description:Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone We used microarrays to detail the global program of dexamethasone regulated gene expression in embryonic neural progenitor/stem cells. Cerebral cortex was isolated from E14.5 mouse fetuses and cultured as neurospheres for 3 passages prior to treatment with 100 nM dexamethasone or ethanol vehicle for 4 hours.

2014-05-21 | E-GEOD-49804 | biostudies-arrayexpress

Studying changes in chromatin accessibility in A549 cells by ATAC-seq directly after 4-hour glucocorticoid treatment and following a 24-hour hormone washout

Project description:We performed ATAC-seq in the A549 cell line. Cells were treated with dexamethasone (100 nM), hydrocortisone (100 nM) or vehicle (ethanol) for 4 hours and either harvested immediately or washed 2x with PBS and subsequently cultured in hormone-free medium for 24 hours before harvest.

2021-05-03 | E-MTAB-9911 | biostudies-arrayexpress

Studying changes in chromatin accessibility in A549 cells by ATAC-seq directly after 20-hour glucocorticoid treatment and following a 24-hour hormone washout

Project description:We performed ATAC-seq in the A549 cell line. Cells were treated with dexamethasone (100 nM), hydrocortisone (100 nM) or vehicle (ethanol) for 20 hours and either harvested immediately or washed 2x with PBS and subsequently cultured in hormone-free medium for 24 hours before harvest.

2021-05-03 | E-MTAB-9910 | biostudies-arrayexpress

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. Total RNA isolated from T47D cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells. Total RNA isolated from uterine leiomyoma cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells.

2011-07-22 | E-GEOD-30871 | biostudies-arrayexpress

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (Expression BeadChip)

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. Keywords: Expression profiling by array Total RNA isolated from T47D cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells. Total RNA isolated from uterine leiomyoma cells subjected to RU486 treatment for 6 hours compared to vehicle (ethanol) treated cells.

2012-09-11 | E-GEOD-40725 | biostudies-arrayexpress

Gene Profile of RU486 effect on LPS induced gene expression in CNS.

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data