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Dev Cell ; 3(6): 877-87, 2002 Dec.
Article in English | MEDLINE | ID: mdl-12479812

ABSTRACT

The mechanisms by which prolactin controls proliferation of mammary epithelial cells (MECs) and morphogenesis of the breast epithelium are poorly understood. We show that cyclin D1(-/-) MECs fail to proliferate in response to prolactin and identify IGF-2 as a downstream target of prolactin signaling that lies upstream of cyclin D1 transcription. Ectopic IGF-2 expression restores alveologenesis in prolactin receptor(-/-) epithelium. Alveologenesis is retarded in IGF-2-deficient MECs. IGF-2 and prolactin receptor mRNAs colocalize in the mammary epithelium. Prolactin induces IGF-2 mRNA and IGF-2 induces cyclin D1 protein in primary MECs. Thus, IGF-2 is a mediator of prolactin-induced alveologenesis; prolactin, IGF-2, and cyclin D1, all of which are overexpressed in breast cancers, are components of a developmental pathway in the mammary gland.


Subject(s)
Cell Division/genetics , Cyclin D1/deficiency , Epithelial Cells/metabolism , Gene Expression Regulation, Developmental/genetics , Insulin-Like Growth Factor II/metabolism , Mammary Glands, Animal/embryology , Prolactin/metabolism , Animals , Breast Neoplasms/genetics , Carcinoma/genetics , Carrier Proteins , Cells, Cultured , Cyclin D1/genetics , Epithelial Cells/cytology , Epithelial Cells/drug effects , Female , Genes/drug effects , Genes/genetics , Genetic Testing , Insulin-Like Growth Factor II/genetics , Mammary Glands, Animal/cytology , Mammary Glands, Animal/metabolism , Membrane Glycoproteins , Mice , Mice, Knockout , Oligonucleotide Array Sequence Analysis , Progesterone/metabolism , Progesterone/pharmacology , Prolactin/genetics , Prolactin/pharmacology , RANK Ligand , RNA, Messenger/genetics , RNA, Messenger/metabolism , Receptor Activator of Nuclear Factor-kappa B , Receptors, Progesterone/deficiency , Receptors, Progesterone/genetics , Signal Transduction/genetics
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