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MiR-203a is differentially expressed during branching morphogenesis and EMT in breast progenitor cells and is a repressor of peroxidasin

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dc.contributor Háskóli Íslands
dc.contributor University of Iceland
dc.contributor.author Briem, Eiríkur
dc.contributor.author Budkova, Zuzana
dc.contributor.author Sigurðardóttir, Anna Karen
dc.contributor.author Hilmarsdóttir, Bylgja
dc.contributor.author Kricker, Jennifer
dc.contributor.author Timp, Winston
dc.contributor.author Magnusson, Magnus Karl
dc.contributor.author Traustadottir, Gunnhildur Asta
dc.contributor.author Gudjonsson, Thorarinn
dc.date.accessioned 2020-05-19T14:16:09Z
dc.date.available 2020-05-19T14:16:09Z
dc.date.issued 2019-02
dc.identifier.citation Briem, E. et al., 2019. MiR-203a is differentially expressed during branching morphogenesis and EMT in breast progenitor cells and is a repressor of peroxidasin. Mechanisms of Development, 155, pp.34–47.
dc.identifier.issn 0925-4773
dc.identifier.uri https://hdl.handle.net/20.500.11815/1818
dc.description Publisher's version
dc.description.abstract MicroRNAs regulate developmental events such as branching morphogenesis, epithelial to mesenchymal transition (EMT) and its reverse process mesenchymal to epithelial transition (MET). In this study, we performed small RNA sequencing of a breast epithelial progenitor cell line (D492), and its mesenchymal derivative (D492M) cultured in three-dimensional microenvironment. Among the most downregulated miRNAs in D492M was miR-203a, a miRNA that plays an important role in epithelial differentiation. Increased expression of miR-203a was seen in D492, concomitant with increased complexity of branching. When miR-203a was overexpressed in D492M, a partial reversion towards epithelial phenotype was seen. Gene expression analysis of D492M and D492MmiR-203a revealed peroxidasin, a collagen IV cross-linker, as the most significantly downregulated gene in D492MmiR-203a. Collectively, we demonstrate that miR-203a expression temporally correlates with branching morphogenesis and is suppressed in D492M. Overexpression of miR-203a in D492M induces a partial MET and reduces the expression of peroxidasin. Furthermore, we demonstrate that miR-203a is a novel repressor of peroxidasin. MiR-203-peroxidasin axis may be an important regulator in branching morphogenesis, EMT/MET and basement membrane remodeling.
dc.description.sponsorship This work was supported by Grants from Landspitali University Hospital Science Fund, University of Iceland Research Fund, and Icelandic Science and Technology Policy - Grant of Excellence: 152144051. ‘Göngum saman’, a supporting group for breast cancer research in Iceland (www.gongumsaman.is). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Primary cells were received from reduction mammoplasty after acquiring informed consent from the donor. Approved by the Icelandic National Bioethics Committee VSN-13-057.
dc.format.extent 34-47
dc.language.iso en
dc.publisher Elsevier BV
dc.relation.ispartofseries Mechanisms of Development;155
dc.rights info:eu-repo/semantics/openAccess
dc.subject Developmental Biology
dc.subject Embryology
dc.subject MicroRNA
dc.subject EMT
dc.subject Þroskunarfræði
dc.subject Fósturfræði
dc.subject Genarannsóknir
dc.title MiR-203a is differentially expressed during branching morphogenesis and EMT in breast progenitor cells and is a repressor of peroxidasin
dc.type info:eu-repo/semantics/article
dcterms.license This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
dc.description.version Peer Reviewed
dc.identifier.journal Mechanisms of Development
dc.identifier.doi 10.1016/j.mod.2018.11.002
dc.relation.url https://www.sciencedirect.com/science/article/pii/S0925477318300972?via%3Dihub
dc.contributor.department Læknadeild (HÍ)
dc.contributor.department Faculty of Medicine (UI)
dc.contributor.department Lífvísindasetur (HÍ)
dc.contributor.department Biomedical Center (UI)
dc.contributor.school Heilbrigðisvísindasvið (HÍ)
dc.contributor.school School of Health Sciences (UI)

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