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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE25314: FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part I) GSE25315: FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part II) Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Roslin Russell

PROVIDER: E-GEOD-25316 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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FOXA1 is a key determinant of estrogen receptor function and endocrine response.

Hurtado Antoni A Holmes Kelly A KA Ross-Innes Caryn S CS Schmidt Dominic D Carroll Jason S JS

Nature genetics 20101212 1

Estrogen receptor-α (ER) is the key feature of most breast cancers and binding of ER to the genome correlates with expression of the Forkhead protein FOXA1 (also called HNF3α). Here we show that FOXA1 is a key determinant that can influence differential interactions between ER and chromatin. Almost all ER-chromatin interactions and gene expression changes depended on the presence of FOXA1 and FOXA1 influenced genome-wide chromatin accessibility. Furthermore, we found that CTCF was an upstream ne ...[more]

PMID: 21151129

Similar Datasets

FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part II)

Project description:Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts. FoxA1 silenced breast cancer MCF-7 cell lines or control siRNA in the presence of Estrogen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen for 6 h. There were three biological replicates for each of the four different groups.

2010-11-17 | E-GEOD-25315 | biostudies-arrayexpress

FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part I)

Project description:Estrogen Receptor-a (ER) is the key feature in the majority of breast cancers and ER binding to the genome correlates with the Forkhead protein FOXA1 (HNF3a), but mechanistic insight is lacking. We now show that FOXA1 is the defining factor that governs differential ER-chromatin interactions. We show that almost all ER-chromatin interactions and gene expression changes are dependent on the presence of FOXA1 and that FOXA1 dictates genome-wide chromatin accessibility. Furthermore, we show that CTCF is an upstream negative regulator of FOXA1-chromatin interactions. In ER responsive breast cancer cells, the dependency on FOXA1 for tamoxifen-ER activity is absolute and in tamoxifen resistant cells, ER binding occurs independently of ligand, but in a FOXA1 dependent manner. Importantly, expression of FOXA1 in non-breast cancer cells is sufficient to alter ER binding and response to endocrine treatment. As such, FOXA1 is the primary determinant that regulates estrogen-ER activity and endocrine response in breast cancer cells and is sufficient to program ER functionality in non-breast cancer contexts. breast cancer MCF-7 cell lines were treaated in the presence of Estrogen, Estrogen plus Tamoxifen, Tamoxifen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen or 1 microM Tamoxifen for 6 h. There were four biological replicates for each of the four different groups.

2010-11-17 | E-GEOD-25314 | biostudies-arrayexpress

Transducin-like enhancer protein 1 mediates estrogen receptor binding and transcriptional activity in breast cancer cells

Project description:Transducin-like enhancer protein 1 mediates estrogen receptor binding and transcriptional activity in breast cancer cells TLE1 silenced breast cancer MCF-7 cell lines or control siRNA in the presence of Estrogen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen (or vehicle) for 6 h. There were six biological replicates for each of the four different groups.

2012-07-23 | E-GEOD-39564 | biostudies-arrayexpress

Genome-wide Mapping of ARRB1 Reveals its Role as a HIF1A Transcriptional Co-regulator and Regulator of Cellular Metabolism [expression array]

Project description:Beta-arrestin 1 (ARRB1) has been implicated in transcriptional regulation as part of protein complexes bound to chromatin. Here we investigate its effect on transcription and its potential impact on prostate cancer. We report the first genome-wide mapping of chromatin binding for ARRB1 and combine it with expression array data to define its transcriptome. We identify Hypoxia Inducible Factor 1A (HIF1A) as a nuclear binding partner that recruits ARRB1 to promoter regions of HIF1A targets. We show that ARRB1 modulates HIF1A-dependent transcription and promotes a shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. In addition, we show that ARRB1 plays an important role in neoplastic transformation, cell growth and resistance to hypoxic stress. This is the first example of an endocytic adaptor protein regulating metabolic pathways and implicates ARRB1 as a tumour promoter. Gene expression of C4-2 cells stably overexpressing ARRB1-GFP or nuclear ARRB1-GFP fusion proteins were compared with the GFP empty vector control or parental C4-2 cell lines using the illumina expression array platform. There were three biological replicates for the control groups and two for each of the ARRB1 groups.

2014-11-26 | E-GEOD-55614 | biostudies-arrayexpress

ARRB1 regulates prostate cancer cell metabolism

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

2014-11-26 | E-GEOD-55616 | biostudies-arrayexpress

RNA interference uncouples the function of a long noncoding RNA product from that of its transcription [SUM159]

Project description:Long noncoding RNAs (lncRNAs) regulate gene expression via their RNA product or through transcriptional interference, yet a strategy to differentiate these two processes is missing. We employed siRNAs to specifically target GNG12-AS1, a lncRNA overlapping the tumour suppressor DIRAS3, transcriptionally or post-transcriptionally. lncRNA transcriptional silencing by siRNA was mediated by Argounate 2 and led to the upregulation of DIRAS3 transcription through switch in RNA polymerase II binding and active histone marks. Conversely, post-transcriptional silencing of GNG12-AS1 had no effect on DIRAS3 expression. Thus, our findings reveal how RNAi machinery can be used to decouple the process and products of lncRNA transcription. The goal of this study was to identify genes regulated by long noncoding RNA GNG12-AS1 in human cells RNA was extracted from human cells (HB2, SUM159) treated with control and GNG12-AS1 siRNAs. The analysis was performed with six biological replicates for each cell line.

2015-11-12 | E-GEOD-60561 | biostudies-arrayexpress

RNA interference uncouples the function of a long noncoding RNA product from that of its transcription [HB2]

2015-11-12 | E-GEOD-60562 | biostudies-arrayexpress

RNA interference uncouples the function of a long noncoding RNA product from that of its transcription: HB2 and SUM159 cells

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

2015-11-12 | E-GEOD-60563 | biostudies-arrayexpress

Autophagy mediates the mitotic senescence transition

Project description:ER:RAS-G12V expressing IMR90 cells were given 100nM 4-OHT and assessed for transcriptional profiling at various time points. IMR90 cells expressing a 4-hydroxytamoxifen (4-OHT) inducible estrogen receptor (ER)-coupled RAS-G12V (ER:RAS-G12V) were given 100nM 4-OHT for these eight time points (0, 2, 8, 24hrs, 2, 4, 6 and 8days) then analysed for transcriptional profiling using the illumina expression array platform (human-6 v2 Expression BeadChips). There were three biological replicates (batch A, B and D) for each of the time points.

2014-07-31 | E-GEOD-59522 | biostudies-arrayexpress

Hes6 expression is controlled by c-Myc and the AR to promote E2F1 activity and poor outcome in castrate-resistant prostate cancer (LNCaP)

Project description:Hes6 is a transcription co-factor that is associated with stem cell characteristics in neural tissue, but its role in cancer remains uncertain. Here we show that Hes6 is controlled by c-Myc and the AR and can drive castration resistance in xenografts of the androgen-dependent LNCaP prostate cancer cell line model. Hes6 activates a cell cycle enhancing transcriptional network that maintains tumour growth in the absence of circulating androgen but with maintained nuclear AR. We demonstrate interaction between E2F1, the AR and Hes6 and show the co-dependency of these factors in the castration-resistant setting. In the clinical setting, we have discovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which could be pharmacologically targeted. LNCaP cells with stable Hes6-overexpression and empty vector controls were grown in RPMI & 10% FBS for 3 days before lysis and extraction of RNA.

2014-04-17 | E-GEOD-36434 | biostudies-arrayexpress

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