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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human MCF7 cells in oestrogen treatment time course.

ABSTRACT: Expression analysis in human MCF7 cells after 3h, 6h or 12h of oestrogen treatment

INSTRUMENT(S): Illumina Human-12 v1 Expreesion BeadChip

ORGANISM(S): Homo sapiens

SUBMITTER: Petra Catalina Schwalie

PROVIDER: E-MTAB-158 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A CTCF-independent role for cohesin in tissue-specific transcription.

Schmidt Dominic D Schwalie Petra C PC Ross-Innes Caryn S CS Hurtado Antoni A Brown Gordon D GD Carroll Jason S JS Flicek Paul P Odom Duncan T DT

Genome research 20100310 5

The cohesin protein complex holds sister chromatids in dividing cells together and is essential for chromosome segregation. Recently, cohesin has been implicated in mediating transcriptional insulation, via its interactions with CTCF. Here, we show in different cell types that cohesin functionally behaves as a tissue-specific transcriptional regulator, independent of CTCF binding. By performing matched genome-wide binding assays (ChIP-seq) in human breast cancer cells (MCF-7), we discovered thou ...[more]

PMID: 20219941

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Comparing oestrogen-responsive genes in endometrial and breast cancer cell lines

Project description:Up to 80% of endometrial and breast cancers express the oestrogen receptor ERa. Unlike breast cancer, anti-oestrogen therapy has had limited success in endometrial cancer, raising the possibility that oestrogen has different effects in the two cancer types. We investigated the role of oestrogen in endometrial and breast cancers using cell lines and found that oestrogen-responsive genes were predominantly unique between the two cancer types.

2018-08-29 | GSE107693 | GEO

Oestrogen promotes innate immune invasion of Candida albicans through inactivation of complement

Project description:Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Roughly, 70% of otherwise healthy women succumb to VVC at least once in their life time. Elevated oestrogen levels are associated with C. albicans colonisation of the vagina and symptomatic infection. However, little is known about how C. albicans adapts to oestrogen. Here, we investigate how adaptation of C. albicans to elevated concentrations of oestrogen on the C. albicans host-pathogen interaction. Growth of C. albicans in physiological relevant concentrations of oestrogen promoted fungal innate immune evasion through reduction of both macrophage and neutrophil phagocytosis. Oestrogen-induced innate immune evasion was mediated via inhibition of opsonophagocytosis through enhanced Gpd2 dependent acquisition of Factor H on the fungal cell surface. The zebrafish larval model of infection confirmed that in vivo oestrogen and Gpd2 promote pathogenicity. Understanding the impact of oestrogen on C. albicans host-pathogen interaction will help improve our knowledge on how oestrogen promotes VVC.

2022-01-04 | GSE145240 | GEO

TLE1 mediates estrogen receptor binding

Project description:Estrogen receptor (ER) binds to distal enhancers within the genome and requires additional factors, such as the Forkhead protein FoxA1, for mediating chromatin interactions. We now show that the human Groucho protein, Transducin-like enhancer protein 1 (TLE1), positively assists some ER-chromatin interactions, a role that is distinct from its general role as a transcriptional repressor. We show that specific silencing of TLE1 inhibits the ability of ER to bind to a subset of ER binding sites within the genome, a phenomenon that results in perturbations in phospho-RNA Pol II recruitment. Furthermore, TLE1 is essential for effective ER-mediated cell division. We have discovered a distinct role for TLE1, as a necessary transcriptional component of the ER complex, where it facilitates ER-chromatin interactions.

2012-11-14 | E-MTAB-1368 | biostudies-arrayexpress

Oestrogen Activates the MAP3K1 Cascade and -catenin to Promote Granulosa-Like Cell Fate in a Human Testis-Derived Cell Line

Project description:: Sex determination triggers the differentiation of the bi-potential gonad into either an ovary or testis. In non-mammalian vertebrates, the presence or absence of oestrogen dictates gonad differ-entiation, while in mammals, this mechanism has been supplanted by the testis determining SRY gene. Exogenous oestrogen can override this genetic trigger to shift somatic cell fate in the gonad towards ovarian developmental pathways by limiting the bioavailability of the key testis factor SOX9 within somatic cells. Our previous work has implicated the MAPK pathway in mediating the rapid cellular response to oestrogen. We performed proteomic and phosphoproteomic anal-yses to investigate the precise mechanism through which oestrogen impacts these pathways to ac-tivate -catenin—a factor essential for ovarian development. We show that oestrogen can activate -catenin within 30 minutes, concomitant with the cytoplasmic retention of SOX9. This occurs through changes to the MAP3K1 cascade, suggesting this pathway is a mechanism through which oestrogen influences gonad somatic cell fate. We demonstrate that oestrogen can promote the shift from SOX9 pro-testis activity to -catenin pro-ovary activity through activation of MAP3K1. Our findings define a previously unknown mechanism through which oestrogen can promote a switch in gonad somatic cell fate and provided novel insights into the impacts of exogenous oestrogen exposure on the testis.

2022-02-17 | PXD026927 | Pride

Effect of oestrogen treatment on growth of human angiomyolipoma xenograft tumours

Project description:SV7tert AML cells were obtained from ATCC and cultured in Dulbecco's modified essential medium (DMEM), glutamine (4mmol) and 10% foetal bovine serum (FBS). Two million SV7tertAML cells were subcutaneously injected into nude mice either with or without subcutaneous oestrogen pellets (n=4 per group); oestrogen was added using 0.36mg 60 day release oestrogen pellets implanted sub-cutaneously. Mice were housed in pathoflex isolators at 26°C, on 12 hour light / dark cycles. Irradiated RB2 diet and autoclaved water provided ad libertum. All oestrogen treated mice inoculated with SV7tertAML cells developed subcutaneous tumours which required termination of the animals at six weeks due to tumour load. These primary tumours were removed and fragments placed subcutaneously in further nude mice which went on to develop tumours both in the presence and absence of oestrogen. Mice were weighed weekly and their clinical condition closely monitored by a trained observer. Mice were terminated individually when the tumour cross-sectional area reached 250mm2 or sooner, which has previously been seen to be below the limit of 10% of initial body weight set by the UKCCCR guidelines. Tumours were removed and a portion flash frozen in liquid nitrogen. RNA was extracted from five tumours from oestrogen treated and control animals. Equal quantities of RNA was pooled and quality checked by Agilent Bioanylyser. Experimenter name = Simon Johnson Experimenter institute = Queens Medical Centre Keywords: estrogen treatment, angiomyolipoma xenograft tumors

2007-09-19 | GSE5868 | GEO

Transcript profiling of oestrogen treatment of primary human neuronal cell cultures

2009-12-01 | GSE17645 | GEO

Oestrogen effects on the left ventricular transcriptome of healhty mice

Project description:Comparison of mouse left ventricular responses to oestrogen with control.

2014-04-10 | E-MEXP-3834 | biostudies-arrayexpress

Transcription profiling of human primary neuronal cell cultures after of oestrogen treatment

Project description:The purpose of this experiment was to identify oestrogen regulated genes in human primary cell cultures of neuronal cells modelling the developing human nervous system. We were especially interested in genes involved in proliferation, differentiation and migration of neuronal cells and genes involved in or linked to neurodegenerative diseases. We have therefore assessed gene expression changes, using Affymetrix GeneChips (HG-U133A), of oestrogen treated human neuronal cell cultures. Experiment Overall Design: Primary neuronal cell cultures were established from human brain tissue, which was obtained from 8-12 weeks old fetuses at legal abortion after informed consent from the patients. Procedures were approved by the local Ethics committee at the Karolinska University Hospital, Stockholm. A total of 28 tissue samples yielding 10 cell cultures were used in this experiment. Half of the cell cultures were treated with 2ÂµM Î²-oestradiol the day after seeding. The duration of the oestrogen treatment was 7 days and the cells were harvested after 8 days of culturing for RNA extraction. Extracted RNA from untreated respectively oestrogen treated cell cultures were pooled yielding two samples, which were each hybridised to Affymetrix microarrys.

2009-12-05 | E-GEOD-17645 | biostudies-arrayexpress

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-05-01 | E-GEOD-39418 | biostudies-arrayexpress

Transcript profiling of oestrogen treatment of primary human neuronal and glial cell cultures

Project description:The purpose of this experiment was to identify oestrogen regulated genes in human primary cell cultures of neuronal and glial cells modelling the developing human nervous system. We were especially interested in genes involved in proliferation, differentiation and migration of neuronal cells and genes involved in or linked to neurodegenerative diseases. We have therefore assessed gene expression changes, using Affymetrix GeneChips (HG-U133A), of oestrogen treated human neuronal/ glial cell cultures. We continued with 14 selected genes and confirmed the gene expression changes, by relative quantitative real time PCR, of 6 genes (p< 0.05) important in neuronal development, three of which also are suggested to have links to neurodegenerative diseases. Keywords: Treatment vs Control

2008-05-28 | GSE10097 | GEO

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