Slug-expressing mouse prostate epithelial cells have increased stem cell potential
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
32590255
DOI
10.1016/j.scr.2020.101844
PII: S1873-5061(20)30145-8
Knihovny.cz E-zdroje
- Klíčová slova
- Epithelial-to-mesenchymal transition, Organoids, Prostate stem cells, Snai2/Slug, Stemness,
- MeSH
- epitelo-mezenchymální tranzice * MeSH
- epitelové buňky MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- pohyb buněk MeSH
- prostata * MeSH
- rodina transkripčních faktorů Snail genetika MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- rodina transkripčních faktorů Snail MeSH
Deciphering the properties of adult stem cells is crucial for understanding of their role in healthy tissue and in cancer progression as well. Both stem cells and cancer stem cells have shown association with epithelial-to-mesenchymal transition (EMT) in various tissue types. Aiming to investigate the epithelial and mesenchymal phenotypic traits in adult mouse prostate, we sorted subpopulations of basal prostate stem cells (mPSCs) and assessed the expression levels of EMT regulators and markers with custom-designed gene expression array. The population of mPSCs defined by a Lin-/Sca-1+CD49fhi/Trop-2+ (LSC Trop-2+) surface phenotype was enriched in mesenchymal markers, especially EMT master regulator Slug, encoded by the Snai2 gene. To further dissect the role of Slug in mPSCs, we used transgenic Snai2tm1.1Wbg reporter mouse strain. Using this model, we confirmed the presence of mesenchymal traits and increase of organoid forming capacity in Slug+ population of mPSCs. The Slug+-derived organoids comprised all prostate epithelial cell types - basal, luminal, and neuroendocrine. Collectively, these data uncover the important role of Slug expression in the physiology of mouse prostate stem cells.
Citace poskytuje Crossref.org
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