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Endocrinology Vol. 141, No. 9 3104-3110
Copyright © 2000 by The Endocrine Society

ARTICLES

Differential Regulation of Insulin-Like Growth Factor-Binding Protein-3 Protease Activity in MCF-7 Breast Cancer Cells by Estrogen and Transforming Growth Factor-ß11

Houta Salahifar, Robert C. Baxter and Janet L. Martin

Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales 2065, Australia

Address all correspondence and requests for reprints to: Dr. Janet Martin, Kolling Institute of Medical Research, Royal North Shore Hospital, St. Leonards, 2065 New South Wales, Australia. E-mail: janetlm{at}med.usyd.edu.au

We have examined the regulation of an insulin-like growth factor-binding protein-3 (IGFBP-3) protease secreted by MCF-7 human breast cancer cells using a ligand-binding assay that relies on the decrease in affinity for des(1–3)IGF-I that occurs when IGFBP-3 becomes proteolyzed. IGFBP-3 protease activity was not altered by treatment of MCF-7 cells with all-trans-retinoic acid, vitamin D, epidermal growth factor, platelet-derived growth factor, insulin, or forskolin. However, estradiol was a potent stimulator of IGFBP-3 protease activity, with a significant and maximal effect at 1 nM. This was prevented by cotreatment with tamoxifen, which had no significant effect in the absence of estradiol. By contrast, TGFß1 dose dependently inhibited the amount of protease activity secreted by MCF-7 cells, with complete reversal of IGFBP-3 degradation apparent in response to 10 ng/ml TGFß1. This study has demonstrated that estrogens and TGFß1, factors that are stimulatory and inhibitory, respectively, for MCF-7 cell growth, also stimulate and inhibit the production of an enzyme capable of proteolyzing the growth inhibitory protein IGFBP-3.




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Copyright © 2000 by The Endocrine Society