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Submitted on June 13, 2002
Accepted on December 16, 2002
1 Mammary Biology and Tumorigenesis Laboratory, National Cancer Institute, NIH, Building 10, Room 5B47, 10 Center Drive, Bethesda, MD 20892-1402 Cancer Research Program, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW, Australia 2010 USDA/ARS Children's Nutrition Research Center, Department of Pediatrics and The Breast Center, Baylor College of Medicine, One Baylor Plaza, MS: 600, Houston, TX 77030
* To whom correspondence should be addressed. E-mail: rhovey{at}zoo.uvm.edu.
PRL (PRL) is a major determinant of mammary epithelial cell proliferation during alveolar development in sexually-mature and pregnant mice. To date it has not been clear whether PRL effects these responses alone, or by also invoking the action of autocrine/paracrine growth factors. In this study we provide evidence that part of the effect of PRL on mammary gland growth is mediated by insulin-like growth factor-II (IGF-II). During sexual maturity and in early pregnancy the level of IGF-II mRNA in the mammary gland was increased concurrent with increased PRL receptor (PRLR) expression. The level of IGF-II mRNA was reduced in mammary tissue from PRLR-/- mice during early pregancy, and explants of mouse mammary gland and HC11 mammary epithelial cells both increased their expression of IGF-II after exposure to PRL in vitro. These findings coincided with the demonstration that IGF-II stimulated alveolar development in mammary glands in whole organ culture. PRL was most efficacious in stimulating IGF-II gene transcription from promoter 3 of the mouse IGF-II gene in vitro. Insight into the mechanism by which PRL induced IGF-II expression was provided by the fact that it was blocked by the Jak2 inhibitor AG490, and the MAP-kinase inhibitor PD98059. Finally, induction of IRS-1 in the mammary glands of PRL-treated mice, and induction of IRS-1 and -2 after treatment with PRL + progesterone indicates that these molecules are induced by PRL as potential signaling intermediates downstream from IGF-I/insulin receptors. Together these data demonstrate a role for IGF-II as a mediator of PRL action in the mouse mammary gland during ductal branching and alveolar development.
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