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Homo sapiens

ABSTRACT: Chromatin enrichment of TRIM24, estrogen receptor and H3K4me2 in estrogen-treated and -untreated MCF7 cells

PROVIDER: PRJNA130083 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR065819.fastq.gz	Fastqsanger.gz
	SRR065820.fastq.gz	Fastqsanger.gz
	SRR065821.fastq.gz	Fastqsanger.gz
	SRR065822.fastq.gz	Fastqsanger.gz
	SRR065823.fastq.gz	Fastqsanger.gz

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Cyclic LSD1 recruitment and dynamic H3K4 methylation establish TRIM24-activated estrogen response

Project description:The role of histone lysine methylation in estrogen receptor-alpha (ERα)-activated transcription is highly context-specific and poorly understood. Here, we show that lysine demethylase 1 (LSD1) mediates loss of H3 lysine 4 dimethylation (H3K4me2) in coordination with tripartite-motif-containing protein 24 (TRIM24)- regulated growth of breaset cancer-derived cells. We performed global profiling of histone H3K4me2 in comparison to genome-wide binding of TRIM24 in MCF7 cells when estrogen is depleted or added. We found specific subsets of genes with functions in transcription and cell proliferation are depleted of H3K4me2 at TRIM24 binding sites. Chromatin immunoprecipitation (ChIP) analyses over a time course of estrogen induction revealed cyclic demethylation of H3K4me2, LSD1, TRIM24 and ERα binding. Inhibition of LSD1 enzymatic activity led to increased H3K4me2 and decreased estrogen response of TRIM24-dependent genes. Additon of a small molecule inhibitor of the TRIM24 bromodomain or depletion of TRIM24 expression amplified the impact of LSD1 inhbition as measured by survival and proliferation of MCF7 cells, suggesting that combinatorial inhibition of LSD1 and TRIM24 may be effective in targeting ER-positive breast cancers.

2019-12-01 | GSE113654 | GEO

Chromatin enrichment of TRIM24, estrogen receptor and H3K4me2 in estrogen-treated and -untreated MCF7 cells

Project description:TRIM24 PHD-Bromo domains exhibit preferential binding to unmethylated H3K4 and acetylated H3K27. TRIM24 is a co-activator of estrogen receptor (ER). The results suggest that specific ER-binding sites are depleted of H3K4me2 with estrogen treatment. TRIM24 binds these sites preferentially and facilitates ER-regulated gene expression, cell survival and proliferation. ChIP performed on MCF7 cells +/- estrogen with antibodies against ER, TRIM24 and H3K4me2. ChIP assays of ER, co-activator TRIM24 and H3K4me2 were performed with two concentrations of antibody, without and 6h with estrogen treatment of MCF7 cells. Antibody-enriched samples were sequenced two times, and compared to an IgG negative control and Input. Enriched DNA sequenced by Illumina Solexa.

2010-09-17 | E-GEOD-24166 | biostudies-arrayexpress

Chromatin enrichment of TRIM24, estrogen receptor and H3K4me2 in estrogen-treated and -untreated MCF7 cells

2010-09-17 | GSE24166 | GEO

Coativator Function Defines the Active Estrogen Receptor Alpha Cistrome

Project description:Genome-wide ChIP-on-Chip against RNA Pol II in untreated MCF7 cells (phenol-red free media) and H3R17me2 in untreated and estrogen (45 min) treated cells.

2009-12-09 | GSE19328 | GEO

Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast cancer

Project description:To investigate the molecular mechanisms by which estrogen receptor α (ERα) inhibits type I IFN-induced signaling. We identified genes induced by ERα signaling using data obtained from RNA-seq of MCF7 cells treated or untreated with selective ERα agonist propyl pyrazole triol (PPT).

2022-05-18 | GSE203058 | GEO

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

Project description:The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that breast cancer cells undergo genome-wide reprogramming of their chromatin landscape, defined by epigenomic maps and chromatin openness, as they acquire resistance to endocrine therapy. This reveals a role for the Notch pathway while excluding classical ERa signaling. In agreement, blocking Notch signaling, using gamma-secretase inhibitors, or targeting its downstream gene PBX1 abrogates growth of endocrine therapy-resistant breast cancer cells. Moreover Notch signaling through PBX1 directs a transcriptional program predictive of tumor outcome and endocrine therapy response. Comparing histone modifications (H3K4me2 and H3K36me3), chromatin openness (FAIRE) and PBX1 binding between endocrine therapy sensitive MCF7 and resistant MCF7-LTED cells.

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Bulk and single cell RNA-seq of MCF7 and MCF7 TDP2-KO cells treated with/without estrogen

Project description:To investigate the function of tyrosyl-DNA phosphodiesterase 2 (TDP2) in estrogen receptor (ER) positive breast cancer, we perfomed bulk and single-cell RNA-seq on MCF7 and MCF7 TDP2-KO cells treated with/without estrogen .

2024-04-17 | GSE225423 | GEO

Genome-wide activity of unliganded Estrogen Receptor alpha in breast cancer cells [ChIP-Seq]

Project description:Estrogen Receptor ? (ER?) has central role in hormone-dependent breast cancer and its ligand-induced functions have been extensively characterized. However, evidence exists that ER? has functions which are independent of ligands. In the present work, we investigated the binding of ER? to chromatin in absence of ligands, and its function(s) on gene regulation. We demonstrated that in MCF7 breast cancer cells unliganded ER? binds to more than four thousands chromatin sites. Unexpectedly, although almost entirely comprised in the larger group of estrogen-induced binding sites, we found that unliganded-ER? binding is specifically linked to genes with developmental functions, as compared to estrogen-induced binding. Moreover, we found that siRNA-mediated downregulation of ER? in absence of estrogen is accompanied by changes in the expression levels of hundreds of coding and noncoding RNAs. Downregulated mRNAs showed enrichment in genes related to epithelial cell growth and development. Stable ER? downregulation using shRNA, which caused cell-growth arrest, was accompanied by increased H3K27me3 at ER? binding sites. Finally, we found that FOXA1 and AP2? binding to several sites is decreased upon ER? silencing, suggesting that unliganded ER? participates, together with other factors, to the maintenance of the luminal-specific cistrome in breast cancer cells. Examination of unligandend estrogen receptor alpha (apoER?) DNA interactions in control and ER? siRNA treated MCF7 cells.

2014-03-03 | E-GEOD-53531 | biostudies-arrayexpress

Gene expression profile in MCF7 breast cancer cells after siRNA knock down of estrogen receptor alpha (ESR1)

Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against estrogen receptor alpha (ESR1). Gene expresion of estrogen receptor alpha (ESR1) was knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with non-targetting control treated cells were analysed using Affymetrix Human Genome U133 Plus 2.0 microarrays.

2012-05-06 | E-GEOD-37820 | biostudies-arrayexpress

Effects of retinoids on estrogen-receptor-positive and -negative breast carcinoma cells: mRNA profiling

Project description:The overall study explores differential sensitivity of estrogen-receptor-positive and -negative breast carcinoma cells to retinoids via gene expression and microRNA profiling in MCF7 and MDA-MB-231 cells. This Series reports results of transcriptional profiling of breast carcinoma cell lines comparing the effects of retinoic acid treatment (6 and 48 hours) on estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. mRNA profiling: Retinoic-acid-treated (1microM) vs vehicle-treated cells, two time points (6 and 48h), two cell lines (MCF7 and MDA-MB-231). Two biological replicates for each condition, balanced dye design.

2010-05-21 | E-GEOD-18390 | biostudies-arrayexpress

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