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Insulin and IGF-1 Induce Different Patterns of Gene Expression in Mouse Fibroblast NIH-3T3 Cells: Identification by cDNA Microarray Analysis

Section on Cellular and Molecular Physiology (J.D., B.-H.Q., D.L.), Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases; Cancer Genetics Branch (J.K., P.M.), National Human Genome Research Institute, National Cancer Institute, Molecular Regulation; and Molecular Oncology Section (L.H.), Pediatric Oncology Branch, NIH, Bethesda, Maryland 20892-1758

Address all correspondence and requests for reprints to: Derek LeRoith, M.D., Ph.D., Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Room 8D12, Building 10, NIH, Bethesda, Maryland 20892-1758. E-mail: derek{at}helix.nih.gov

The IGF-1 receptor and the related insulin receptor are similar in structure and activate many of the same postreceptor signaling pathways, yet they mediate distinct biological functions. It is still not understood how the specificity of insulin vs. IGF-1 signaling is controlled. In this study, we have used cDNA microarrays to monitor the gene expression patterns that are regulated by insulin and IGF-1. Mouse fibroblast NIH-3T3 cells expressing either the wild-type human IGF receptor or the insulin receptor were stimulated with either IGF-1 or insulin, respectively. Thirty genes, 27 of which were not previously known to be IGF-1 responsive, were up-regulated by IGF-1 but not by insulin. Nine genes, none of which was previously known to be insulin responsive, were up-regulated by insulin but not by IGF-1. The IGF- and insulin-induced regulation of 10 of these genes was confirmed by Northern blot analysis. Interestingly, more than half of the genes up-regulated by IGF-1 are associated with mitogenesis and differentiation, whereas none of the genes specifically up-regulated by insulin are associated with these processes. Our results indicate that under the conditions used in this study, IGF-1 is a more potent activator of the mitogenic pathway than insulin in mouse fibroblast NIH-3T3 cells.

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