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research article

Progesterone and Wnt4 control mammary stem cells via myoepithelial crosstalk

Rajaram, Renuga Devi
•
Buric, Duje  
•
Caikovski, Marian  
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2015
Embo Journal

Ovarian hormones increase breast cancer risk by poorly understood mechanisms. We assess the role of progesterone on global stem cell function by serially transplanting mouse mammary epithelia. Progesterone receptor (PR) deletion severely reduces the regeneration capacity of the mammary epithelium. The PR target, receptor activator of Nf-kB ligand (RANKL), is not required for this function, and the deletion of Wnt4 reduces the mammary regeneration capacity even more than PR ablation. A fluorescent reporter reveals so far undetected perinatal Wnt4 expression that is independent of hormone signaling. Pubertal and adult Wnt4 expression is specific to PR+ luminal cells and requires intact PR signaling. Conditional deletion of Wnt4 reveals that this early, previously unappreciated, Wnt4 expression is functionally important. We provide genetic evidence that canonical Wnt signaling in the myoepithelium required PR and Wnt4, whereas the canonical Wnt signaling activities observed in the embryonic mammary bud and in the stroma around terminal end buds are independent of Wnt4. Thus, progesterone and Wnt4 control stem cell function through a luminal-myoepithelial crosstalk with Wnt4 acting independent of PR perinatally.

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Type
research article
DOI
10.15252/embj.201490434
Web of Science ID

WOS:000350693400006

PubMed ID

25603931

Author(s)
Rajaram, Renuga Devi
Buric, Duje  
Caikovski, Marian  
Ayyanan, Ayyakkannu
Rougemont, Jacques  
Shan, Jingdong
Vainio, Seppo J.
Yalcin-Ozuysal, Ozden
Brisken, Cathrin  
Date Issued

2015

Publisher

Wiley-Blackwell

Published in
Embo Journal
Volume

34

Issue

5

Start page

641

End page

652

Subjects

canonical Wnt signaling

•

hormones

•

mammary stem cells

•

myoepithelium

•

paracrine

Editorial or Peer reviewed

REVIEWED

Written at

EPFL

EPFL units
UPBRI  
BICC  
Available on Infoscience
April 13, 2015
Use this identifier to reference this record
https://infoscience.epfl.ch/handle/20.500.14299/113182
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