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Evaluating hormone responses in Esr1-wildtype and mutant mammary luminal cells [RNA-seq]

ABSTRACT: Evaluating hormone responses in Esr1-wildtype and mutant mammary luminal cells [RNA-seq]

PROVIDER: PRJNA773928 | ENA |

REPOSITORIES: ENA

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Evaluating hormone responses in Esr1-wildtype and mutant mammary luminal cells [RNA-seq]

Project description:To examine the effects of hormone stimulation on Esr1-wildtype and Esr1-mutant mammary glands, we will ovariectomize both wildtype and ER-mutant mice. Following ovariectomy (OVX), animals will be implanted with hormone pellets (either placebo, estrogen, and/or progesterone). Then, we perform RNA-seq on FACS-sorted mature luminal cells (ML) from mammary glands of treated mice. This analysis will allow for separation of ER mutant-intrinsic effects on gene expression vs. combinatorial effects from exposure to either estrogen or progesterone.

2023-05-07 | GSE186453 | GEO

Evaluating ER-alpha and PR interactions with chromatin in Esr1-wildtype and mutant mammary luminal cells

Project description:Evaluating ER-alpha and PR interactions with chromatin in Esr1-wildtype and mutant mammary luminal cells

| PRJNA773929 | ENA

Evaluating ER-alpha and PR interactions with chromatin in Esr1-wildtype and mutant mammary luminal cells

Project description:To understand the interactions between ER-alpha and PR interactions with chromatin in Esr1-wildtype versus mutant mammary cells, ChIP-seq was performed against both transcription factors. Animals were treated for four days with E2 and P4, then harvested for analysis.

2023-05-07 | GSE186452 | GEO

Evaluating an Esr1-mutant novel cell population emerging upon ERα-antagonism by bulk ATAC-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, individual mammary epithelial cell populations were FACS-isolated and sequenced.

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.

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ESR1+ luminal epithelial cells contribute to androgen-independent prostate survival in the absence of SRD5A2

Project description:Steroid 5α reductase 2 (SRD5A2) is crucial for prostatic development, converting testosterone to dihydrotestosterone (DHT). While 5α reductase inhibitors (5ARI) effectively reduce prostate size in benign prostate hyperplasia (BPH), their limited efficacy against BPH-related lower urinary tract symptoms (LUTS) and mechanisms of 5ARI resistance remain unclear. Here, we developed a Srd5a2-/- mouse model and employed single-cell RNA sequencing (scRNA-seq) to explore the impact of SRD5A2 absence on prostate cellular heterogeneity. Significant alterations in luminal epithelial (LE) populations were observed, alongside increased proportion and proliferative phenotype of estrogen receptor 1 (ESR1)+ Luminal Epithelia 2 (LE2) cells, following an SRD5A2-independent ESR1 differentiation trajectory. LE2 cells exhibited enhanced estrogen response gene signatures, suggesting alternative pathways for prostate growth without SRD5A2. Human prostate biopsy analysis revealed an inverse correlation between SRD5A2 expression and LE2 markers (ESR1 and PKCα). These findings provide insights into prostate biology, 5ARI resistance mechanisms, and potential targeted therapies for BPH-related LUTS.

2023-06-26 | GSE235514 | GEO

Maintenance of Hormone Responsiveness in Luminal Breast Cancers by Suppression of Notch

Project description:Luminal breast cancers express estrogen (ER) and/or progesterone (PR) receptors and respond to hormone therapies. Basal-like “triple negative” (TN) cancers lack steroid receptors but are cytokeratin (CK) 5-positive and require chemotherapy. Here we show that over half of primary ER+PR+ breast cancers contain an ER–PR–CK5+ “luminobasal” subpopulation exceeding 1% of cells. Starting from ER+PR+ luminal cell lines, we generated novel lines with varying luminal to luminobasal-cell ratios and studied their molecular and biological properties. In luminal disease, luminobasal cells expand in response to antiestrogen or estrogen withdrawal therapies. The phenotype and gene signature of the hormone resistant cells matches that of clinical TN basal-like and claudin-low disease. Luminobasal-cell expansion in response to hormone therapies is regulated by Notch1 signaling and can be blocked by gamma-secretase inhibitors (GSI). Our data establish a previously unrecognized plasticity of ER+PR+ luminal breast cancers that, without genetic manipulation, mobilizes outgrowth of hormone-resistant basal-like disease in response to treatment. This undesirable outcome can be prevented by combining endocrine therapies with Notch inhibition. 24 array samples

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Maintenance of Hormone Responsiveness in Luminal Breast Cancers by Suppression of Notch

2011-12-21 | GSE31870 | GEO

T47D cell line transfected with various ESR1 fusion genes (or with estrogen treatment), vs. YFP transfection alone

Project description:Gene expression profiling of the downstream transcriptional changes induced by ESR1 fusion genes observed in human breast tumors resistant to hormone therapy Experimental T47D cells stably expressing ESR1 fusion genes (or T47D cells treated with estradiol) vs. T47D cells expressing YFP

2015-06-12 | E-GEOD-69774 | biostudies-arrayexpress

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