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

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

PROVIDER: PRJNA986171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24985050_1.fastq.gz	Fastqsanger.gz
	SRR24985050_2.fastq.gz	Fastqsanger.gz
	SRR24985051_1.fastq.gz	Fastqsanger.gz
	SRR24985051_2.fastq.gz	Fastqsanger.gz
	SRR24985052_1.fastq.gz	Fastqsanger.gz

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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

Differentiated prostate luminal cells acquire enhanced regenerative potential after androgen ablation

Project description:Cells in the prostate are postulated to have stem cell properties based on organ regeneration following castration. Through single cell RNA-seq (scRNA-Seq) analysis, we identify a rare luminal cell population in the mouse prostate that expresses stem-like markers (Sca1+, Psca+), as well as a larger population of more differentiated cells (Nkx3.1+, Pbsn+, CD133/Prom1+). Unexpectedly, both populations acquire enhanced organoid regeneration potential following castration and contribute equipotently to prostatic regeneration, as revealed by lineage tracing. Regeneration is mediated, in part, by androgen-driven expression of Nrg2, Igf1, Fgf10 and Rspo3 by distinct populations of mesenchymal cells acting in a paracrine fashion on luminal cells. Human prostate tissue contains similar differentiated and stem-like luminal subpopulations which also, collectively. acquire enhanced regenerative potential after androgen ablation therapy. Thus, nearly all luminal cells that persist post-castration contribute to prostate regeneration, not just rare stem cells.

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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.

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Luminal Androgen Receptor-Enriched tripple Negative Breast Cancer

Project description:Luminal Androgen Receptor-Enriched tripple Negative Breast Cancer

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Luminal Androgen Receptor-Enriched tripple Negative Breast Cancer

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ESR1 and p53 Interactome Defines Mechanisms of Therapeutic Response to Tamoxifen Therapy in Luminal Breast Cancer Patients

Project description:The canonical mechanism behind tamoxifen (Tam)’s therapeutic effect on estrogen receptor  /ESR1+ breast cancers is inhibition of ESR1-dependent estrogen signaling. Although ESR1+ tumors expressing wild-type p53 were reported to be more responsive to Tam therapy, p53 has not been factored into choice of this therapy and the mechanism underlying the role of p53 in Tam response remain unclear. In a window of opportunity trial on patients with newly diagnosed stage I-III ESR1+/HER2/ wild-type p53 –breast cancer who were randomized to arms with or without Tam prior to surgery, we reveal that the ESR1-p53 interaction in tumors was inhibited by Tam. This resulted in functional reactivation of p53 leading to transcriptional reprogramming that favors tumor suppressive signaling, as well as downregulation of oncogenic pathways. These findings illustrating the convergence of ESR1 and p53 signaling during Tam therapy contribute to mechanistic understanding of the impact of p53 on the response to Tam therapy.

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Project description:A subpopulation of prostate luminal epithelial cells has been previously reported to be sufficient to regenerate prostatic architecture following consecutive rounds of androgen deprivation/repletion. This functional characteristic suggest prostate luminal epithelial cells as the putative cell-of-origin for castration-resistant prostate cancer - which more notizable fenotype is the lack of response to androgen deprivation thereapy. We used microarrays to profile the androgen-induced transcripts in luminal prostate epithelial cells involved in a cycle of prostate regression/regeneration in Hoxb13-rtTA|TetO-H2BGFP transgenic mice.

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Project description:Differentiated prostate luminal cells acquire enhanced regenerative potential after androgen ablation

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esr1-drn-Transcriptomic study of the transcription factor ESR1/DRN.

Project description:adt06-01_esr1-drn_dexamethasone - esr1-drn - Identification of the target genes of the ESR1/DRN TF using dexamethasone induction - Identification of the target genes of the ESR1/DRN TF using dexamethasone induction Keywords: normal vs transgenic comparison 5 dye-swap - CATMA arrays

2008-09-25 | E-GEOD-12919 | biostudies-arrayexpress

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