scholarly journals Changes in the cytologic distribution of heparin/heparan sulfate interacting protein/ribosomal protein L29 (HIP/RPL29) during in vivo and in vitro mouse mammary epithelial cell expression and differentiation

2002 ◽  
Vol 223 (1) ◽  
pp. 70-84 ◽  
Author(s):  
Catherine B. Kirn-Safran ◽  
Joanne Julian ◽  
Jennifer E. Fongemie ◽  
David E. Hoke ◽  
Kirk J.C. Czymmek ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Heparan Sulfate ◽  
Ribosomal Protein ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Interacting Protein ◽  
Mouse Mammary Epithelial Cell ◽  
Cell Expression

scholarly journals Mammary epithelial cell phenotype disruption in vitro and in vivo through ERalpha36 overexpression

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173931 ◽  
Author(s):  
Charlène Thiebaut ◽  
Clémence Chamard-Jovenin ◽  
Amand Chesnel ◽  
Chloé Morel ◽  
El-Hadi Djermoune ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Cell Phenotype

scholarly journals A Dual Role for Oncostatin M Signaling in the Differentiation and Death of Mammary Epithelial Cells in Vivo

2008 ◽  
Vol 22 (12) ◽  
pp. 2677-2688 ◽  
Author(s):  
Paul G. Tiffen ◽  
Nader Omidvar ◽  
Nuria Marquez-Almuina ◽  
Dawn Croston ◽  
Christine J. Watson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Oncostatin M ◽  
Specific Gene ◽  
Mammary Involution

Abstract Recent studies in breast cancer cell lines have shown that oncostatin M (OSM) not only inhibits proliferation but also promotes cell detachment and enhances cell motility. In this study, we have looked at the role of OSM signaling in nontransformed mouse mammary epithelial cells in vitro using the KIM-2 mammary epithelial cell line and in vivo using OSM receptor (OSMR)-deficient mice. OSM and its receptor were up-regulated approximately 2 d after the onset of postlactational mammary regression, in response to leukemia inhibitory factor (LIF)-induced signal transducer and activator of transcription-3 (STAT3). This resulted in sustained STAT3 activity, increased epithelial apoptosis, and enhanced clearance of epithelial structures during the remodeling phase of mammary involution. Concurrently, OSM signaling precipitated the dephosphorylation of STAT5 and repressed expression of the milk protein genes β-casein and whey acidic protein (WAP). Similarly, during pregnancy, OSM signaling suppressed β-casein and WAP gene expression. In vitro, OSM but not LIF persistently down-regulated phosphorylated (p)-STAT5, even in the continued presence of prolactin. OSM also promoted the expression of metalloproteinases MMP3, MMP12, and MMP14, which, in vitro, were responsible for OSM-specific apoptosis. Thus, the sequential activation of IL-6-related cytokines during mammary involution culminates in an OSM-dependent repression of epithelial-specific gene expression and the potentiation of epithelial cell extinction mediated, at least in part, by the reciprocal regulation of p-STAT5 and p-STAT3.

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