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The STAT5-regulated miR-193b locus restrains mammary stem and progenitor cell activity and alveolar differentiation

Authors
Yoo, Kyung HyunKang, KeunsooFeuermann, YonatanJang, Seung JinRobinson, Gertraud W.Hennighausen, Lothar
Issue Date
Nov-2014
Publisher
Academic Press
Citation
DEVELOPMENTAL BIOLOGY, v.395, no.2, pp 245 - 254
Pages
10
Journal Title
DEVELOPMENTAL BIOLOGY
Volume
395
Number
2
Start Page
245
End Page
254
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/147250
DOI
10.1016/j.ydbio.2014.09.012
ISSN
0012-1606
1095-564X
Abstract
The transcription factor STAT5 mediates prolactin signaling and controls functional development of mammary tissue during pregnancy. This study has identified the miR-193b locus, also encoding miRNAs 365-1 and 6365, as a STAT5 target in mammary epithelium. While the locus was characterized by active histone marks in mammary tissue, STAT5 binding and expression during pregnancy, it was silent in most non-mammary cells. Inactivation of the miR-193b locus in mice resulted in elevated mammary stem/progenitor cell activity as judged by limiting dilution transplantation experiments of primary mammary epithelial cells. Colonies formed by mutant cells were larger and contained more Ki-67 positive cells. Differentiation of mammary epithelium lacking the miR-193b locus was accelerated during puberty and pregnancy, which coincided with the loss of Cav3 and elevated levels of Elf5. Normal colony development was partially obtained upon ectopically expressing Cav3 or upon siRNA-mediated reduction of Elf5 in miR-193b-null primary mammary epithelial cells. This study reveals a previously unknown link between the mammary-defining transcription factor STAT5 and a microRNA cluster in controlling mammary epithelial differentiation and the activity of mammary stem and progenitor cells. Published by Elsevier Inc.
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