Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/5967
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dc.contributor.authorRajaram, Renuga Devi-
dc.contributor.authorBuric, Duje-
dc.contributor.authorCaikovski, Marian-
dc.contributor.authorAyyanan, Ayyakkannu-
dc.contributor.authorRougemont, Jacques-
dc.contributor.authorShan, Jingdong-
dc.contributor.authorVainio, Seppo J.-
dc.contributor.authorYalçın Özuysal, Özden-
dc.contributor.authorBrisken, Cathrin-
dc.date.accessioned2017-07-19T13:09:18Z
dc.date.available2017-07-19T13:09:18Z
dc.date.issued2015-03-04
dc.identifier.citationRajaram, R.D., Buric, D., Caikovski, M., Ayyanan, A., Rougemont, J., Shan, J., Vainio, S.J., Yalçın Özuysal, Ö., and Brisken, C. (2015). Progesterone and Wnt4 control mammary stem cells via myoepithelial crosstalk. EMBO Journal, 34(5), 641-652. doi:10.15252/embj.201490434en_US
dc.identifier.issn0261-4189
dc.identifier.issn0261-4189-
dc.identifier.urihttps://doi.org/10.15252/embj.201490434
dc.identifier.urihttp://hdl.handle.net/11147/5967
dc.description.abstractOvarian 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-κB 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. Synopsis This paper ascribes a new role for Wnt4 in pre-pubertal mammary gland development while revealing luminal cells to respond to Wnt activation. During regeneration, Wnt4 interacts with progesterone receptor signaling, correcting previous notions on RANKL signaling in this context. Wnt4 is an essential control factor for mammary epithelial stem cell function. RANKL is not required for mammary gland regeneration potential. Wnt4 activates canonical Wnt signaling in the basal/myoepithelial compartment. Progesterone receptor signaling is required for mammary epithelial Wnt4 expression already during puberty. This paper ascribes a new role for Wnt4 in pre-pubertal mammary gland development while revealing luminal cells to respond to Wnt activation. During regeneration, Wnt4 interacts with progesterone receptor signaling, correcting previous notions on RANKL signaling in this context.en_US
dc.description.sponsorshipSwiss National Center of Competence in Research (NCCR) in Molecular Oncology (SNF3100A0-112090); Marie Heim-Vogtlin fellowship from Swiss National Science Foundation (MHV - PMPDP3_129024); Academy of Finland (206038--121647--251314); Sigrid Juselius Foundation; Novonordisk Fonden; European Union (LSHG-CT-2004-005085-HEALTH-F5-2008-223007 STAR-T REK EURenOmics)en_US
dc.language.isoenen_US
dc.publisherJohn Wiley and Sons Inc.en_US
dc.relation.ispartofEMBO Journalen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCanonical Wnt signalingen_US
dc.subjectHormonesen_US
dc.subjectMammary stem cellsen_US
dc.subjectMyoepitheliumen_US
dc.subjectParacrineen_US
dc.subjectWnt4 proteinen_US
dc.titleProgesterone and Wnt4 control mammary stem cells via myoepithelial crosstalken_US
dc.typeArticleen_US
dc.authoridTR103812en_US
dc.institutionauthorYalçın Özuysal, Özden-
dc.departmentIzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume34en_US
dc.identifier.issue5en_US
dc.identifier.startpage641en_US
dc.identifier.endpage652en_US
dc.identifier.wosWOS:000350693400006
dc.identifier.scopusSCOPUS:2-s2.0-84924023108
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.15252/embj.201490434-
dc.relation.doi10.15252/embj.201490434en_US
dc.coverage.doi10.15252/embj.201490434en_US
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeArticle-
item.grantfulltextopen-
item.languageiso639-1en-
item.fulltextWith Fulltext-
crisitem.author.deptDepartment of Molecular Biology and Genetics-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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