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Evaluating the presence of rare ERα-antagonism induced cells in WT tissues

ABSTRACT: Evaluating the presence of rare ERα-antagonism induced cells in WT tissues

PROVIDER: PRJNA846353 | ENA |

REPOSITORIES: ENA

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Evaluating the presence of rare ERα-antagonism induced cells in WT tissues

Project description:To examine the effects of ERα antagonism (giredestrant) on Esr1-wildtype and Esr1-mutant mammary glands, animals were treated with hormone pellets (E2, P4), then dosed daily with vehicle (MCT) or giredestrant (30 mg/kg, p.o.) for four days. Following dosing, individual mammary epithelial cell populations were FACS-isolated and sequenced. Rare giredestrant-induced novel cells (at least 1000 cells per sample) were collected from WT tissues and compared to mutant-induced novel cells.

2024-10-31 | GSE205577 | GEO

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk ATAC-seq

2024-10-31 | GSE205576 | GEO

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk RNA-seq

2024-10-31 | GSE205575 | GEO

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by single RNA-seq

Project description:To examine the effects of ERα antagonism (giredestrant) on Esr1-wildtype and Esr1-mutant mammary glands, animals were treated with hormone pellets (E2, P4), then dosed daily with vehicle (MCT) or giredestrant (30 mg/kg, p.o.) for four days. Following dosing, EpCAM+ cells were isolated and used for single cell sequencing. For each condition, cells from 2 animals were pooled for sequencing.

2024-10-31 | GSE205573 | GEO

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by single RNA-seq

Project description:Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by single RNA-seq

| PRJNA846351 | ENA

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk RNA-seq

Project description:Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk RNA-seq

| PRJNA846355 | ENA

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk ATAC-seq

Project description:Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk ATAC-seq

| PRJNA846354 | ENA

Functional effect of DOT1L pharmacological inhibition in ERα-positive Ovarian Cancer cells

Project description:Estrogen Receptor alpha (ERα), a nuclear receptor with transcriptional activity, is a master regulator of estrogen signaling, widely known as therapeutic target in hormone-responsive breast cancer (BC). Moreover, ERα is highly expressed in approximately 80% of High Grade Serous Ovarian Cancer (HGSOC), the most common epithelial ovarian carcinoma. Despite some promising clinical trials evaluating endocrine therapy in this type of tumor, the role of ERα is still unknown. Epigenetic changes, such as DNA methylation, are emerging as key contributing factors to carcinogenesis. Disruptor of telomeric silencing-1-like (DOT1L), the only known histone methyl transferase capable to produce H3K79 mono, di and tri-methylation, modulates ERα actions in hormone-responsive BC. Considering this evidence, ERα-DOT1L association was confirmed in ERα-positive OC cells, PEO1 and PEO4, by Co-IP. DOT1L pharmacological inhibition by EPZ004777 (EPZ) revealed the involvement of this epigenetic enzyme in cell proliferation, cell cycle progression and apoptosis. Transcriptome profiling after ICI (a Selective Estrogen Receptor Degrader) and EPZ treatment, in both cell lines, has underlined a deep impact of both compounds on ERα-modulated genes, including the down-regulation of ERα itself. On the other hand, functional analysis showed that commonly affected transcripts are involved in different cellular processes, such as cancer cell survival, chemoresistance and cell cycle progression. Moreover, ChIP-qPCR performed on ERα promoter highlighted ERα and DOT1L co-localization, both in PEO1 and in PEO4 cells, which was reduced after EPZ treatment, suggesting a role of this complex on receptor transcriptional activity. In addition, drug combination studies performed with EPZ and ICI showed an additive effect in cell growth inhibition. Taken together, these results suggest DOT1L as a potential therapeutic target in the treatment of OC.

2019-11-04 | E-MTAB-8198 | biostudies-arrayexpress

Genome-wide analysis of SRC-1/NCOA1 and Erα/ESR1 binding in chromatin obtained from the ERα stably transfected U2OS osteosarcoma cell line (U2OS-ERα) with ChIP-SEQ.

Project description:To better understand the role of SRC-1 in estrogen signaling in bone, a genome-wide analysis of ERα and SRC-1 binding sites in the absense and presence of E2 was conducted.

2016-12-04 | GSE26110 | GEO

A super enhancer-controlled BRD4/ERα-RET-ERα positive feedback loop promotes ERα-positive breast cancer [GRO-seq]

Project description:Dysregulated estrogen and estrogen receptor (ER)-induced gene transcription is tightly associated with estrogen receptor alpha (ERα)-positive breast carcinogenesis. ERα-occupied enhancers, particularly super enhancers, have been suggested to play a vital role in such transcriptional events. However, the landscape of ERα-occupied super enhancers (ERSEs) as well as key super enhancer-associated genes remain to be fully characterized. Here, we defined the landscape of ERSEs in MCF7, a ERα-positive breast cancer cell line, and demonstrated that bromodomain protein BRD4 is a master regulator of the transcriptional activation of ERSE and cognate ERα-target genes. Furthermore, RET, a member of the tyrosine protein kinase family of proteins, was identified to be a key target gene of BRD4-regulated ERSEs, which is vital for estrogen/ ERα-induced gene transcriptional activation and malignant phenotypes through activating the Ras-Raf-MEK-ERK-p90RSK-ERα phosphorylation cascade. Accordingly, combination therapy with BRD4 and RET inhibitors exhibited synergistic effects on suppressing ERα-positive breast cancer both in vitro and in vivo. Taken together, our data uncovered the critical role of a super enhancer-associated BRD4/ERα-RET-ERα positive feedback loop in ERα-positive breast cancer, and targeting components in this loop will provide new therapeutic avenue for treating ERα-positive breast cancer in the clinic.

2022-10-19 | GSE186643 | GEO

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