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ABSTRACT: Prostatic stromal tumor

PROVIDER: PRJNA491295 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7848660_1.fastq.gz	Fastqsanger.gz
	SRR7848660_2.fastq.gz	Fastqsanger.gz
	SRR7848661_1.fastq.gz	Fastqsanger.gz
	SRR7848661_2.fastq.gz	Fastqsanger.gz
	SRR7848662_1.fastq.gz	Fastqsanger.gz

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Project description:Androgen-signaling is essential for prostate development. However, how androgen action facilitates prostatic stem/progenitor initiated pubertal prostatic growth remains unclear. Here, we demonstrate that androgens regulate Shh-signaling to control the cellular niche in prostatic epithelial development. Selective deletion of androgen receptor (AR) in stromal Shh-responsive cells significantly impedes pubertal prostatic epithelial morphogenesis and growth. Dysregulation of developmental signaling networks revealed in both prostatic stromal and epithelial cells of AR-deficient mice. Specifically, deletion of AR yielded increased Gli1 expression in prostatic stromal cells, elevated Shh expression in adjacent epithelial cells and stark inhibition of prostate cell growth. Trajectory analysis revealed AR deletion induces abnormal differentiation patterns of prostatic epithelia. Recombination of prostatic epithelial cells with AR-deficient stromal Gli1-expressing cells fails to develop normal prostatic epithelia. These data demonstrate the decisive role of stromal AR in interacting with Shh-signaling in the cellular niche to control pubertal prostatic morphogenesis and growth.

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Project description:The heterogeneity of the prostate stromal cells is widely appreciated but the functional implication remains incompletely understood. Using genetic lineage tracing and light-sheet imaging, we show that some fibroblast cells near the junction of the mouse proximal prostatic ducts and prostatic urethra highly express Lgr5. Genetic ablation of these anatomically restricted stromal cells, but not nonselective ablation of prostatic stromal cells, rapidly induces prostate epithelial turnover and dedifferentiation that are reversed following spontaneous restoration of the Lgr5+ stromal cells. These changes are not mediated via endocrine or nervous regulation but can be phenocopied by physical disruption of prostatic lumen integrity. RNA-Seq analysis implies that ablating the Lgr5+ stromal cells activates a mechanosensory response, which is supported by increased prostate tissue stiffness and activation of the mitogen-activated protein kinase (MAPK). Suppressing MAPK overrides the increased epithelial proliferation. This study demonstrates that the Lgr5+ stromal cells regulate tissue homeostasis in a long-distance manner by maintaining anatomic integrity and implies that the cells near the transitional regions between organs likely control organ homeostasis by sustaining a balanced mechanoforce.

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