Prolactin does not require insulin-like growth factor intermediates but synergizes with insulin-like growth factor I in human breast cancer cells.

Molecular Cancer Research : MCR
Kristopher C Carver, Linda A Schuler

Abstract

Insulin-like growth factor (IGF)-II is a required intermediate for prolactin-induced up-regulation of cyclin D1 and proliferation in normal murine mammary epithelial cells in vivo and in vitro. However, we have recently shown that prolactin can rapidly induce cyclin D1 protein expression and subsequent proliferation in the MCF-7 human breast cancer cell line, suggesting that prolactin actions can be independent of IGFs in breast disease. Here, we investigate the relationship between these factors and show that prolactin up-regulated transcript levels of both IGF-I and IGF-II, but only after increases in cyclin D1 protein were observed. Moreover, prolactin increased cyclin D1 in the presence of the IGF-I receptor neutralizing antibody alphaIR3. However, on cotreatment, IGF-I and prolactin elicited cooperative phosphorylation of extracellular signal-regulated kinases 1 and 2 and protein kinase B/AKT, but not signal transducer and activator of transcription 5. This interaction extended to increased activation of activating protein-1 enhancer elements, phosphorylation of glycogen synthase kinase 3beta, induction of cyclin D1, and ultimately, increased cell number. It also increased invasive behavior, which correlated with elevated ...Continue Reading

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Citations

Jul 17, 2009·Lab on a Chip·Keil J RegehrDavid J Beebe
Feb 1, 2011·Breast Cancer Research : BCR·Lisa M ArendtLinda A Schuler
Jun 6, 2015·Biochemical and Biophysical Research Communications·Alan HammerMaria Diakonova
Jun 16, 2009·Molecular and Cellular Endocrinology·Kristopher C CarverLinda A Schuler
Jan 1, 2011·Expert Review of Endocrinology & Metabolism·Yash ChhabraAndrew J Brooks
Mar 27, 2013·The Journal of Biological Chemistry·Craig E BarcusLinda A Schuler

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