NDLI: Potentiation of Growth Factor Signaling by Insulin-like Growth Factor-binding Protein-3 in Breast Epithelial Cells Requires Sphingosine Kinase Activity

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Potentiation of Growth Factor Signaling by Insulin-like Growth Factor-binding Protein-3 in Breast Epithelial Cells Requires Sphingosine Kinase Activity

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Potentiation of Growth Factor Signaling by Insulin-like Growth Factor-binding Protein-3 in Breast Epithelial Cells Requires Sphingosine Kinase Activity

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lin, Mike Z. Martin, Janet L. Baxter, Robert C. Mcgowan, Eileen M.
Description	Author Affiliation: Martin JL ( Hormones and Cancer Group, Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales 2065, Australia. janetlm@med.usyd.edu.au)
Abstract	We have investigated the mechanism underlying potentiation of epidermal growth factor receptor (EGFR) and type 1 insulin-like growth factor receptor (IGFR1) signaling by IGF-binding protein-3 (IGFBP-3) in MCF-10A breast epithelial cells, focusing on a possible involvement of the sphingosine kinase (SphK) system. IGFBP-3 potentiated EGF-stimulated EGF receptor activation and DNA synthesis, and this was blocked by inhibitors of SphK activity or small interference RNA-mediated silencing of SphK1, but not SphK2, expression. Similarly, IGFR1 phosphorylation and DNA synthesis stimulated by LR3-IGF-I (an IGF-I analog not bound by IGFBP-3), were enhanced by IGFBP-3, and this was blocked by SphK1 silencing. SphK1 expression and activity were stimulated by IGFBP-3 approximately 2-fold over 24 h. Silencing of sphingosine 1-phosphate receptor 1 (S1P1) or S1P3, but not S1P2, abolished the effect of IGFBP-3 on EGF-stimulated EGFR activation. The effects of IGFBP-3 could be reproduced with exogenous S1P or medium conditioned by cells treated with IGFBP-3, and this was also blocked by inhibition of S1P1 and S1P3. These data indicate that potentiation of growth factor signaling by IGFBP-3 in MCF-10A cells requires SphK1 activity and S1P1/S1P3, suggesting that S1P, the product of SphK activity and ligand for S1P1 and S1P3, is the 'missing link' mediating IGF and EGFR transactivation and cell growth stimulation by IGFBP-3.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	38
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-09-18
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Breast Metabolism Epithelial Cells Insulin-Like Growth Factor Binding Proteins Insulin-Like Growth Factor I Phosphotransferases (Alcohol Group Acceptor) Signal Transduction Physiology Cytology Cell Line, Tumor DNA Biosynthesis Enzyme Activation Gene Silencing Insulin-Like Growth Factor Binding Protein 3 Lysophospholipids RNA, Small Interfering Receptor, Epidermal Growth Factor Receptor, IGF Type 1 Receptors, Lysosphingolipid Sphingosine Analogs & Derivatives Transcriptional Activation Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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