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J Biol Chem, Vol. 274, Issue 25, 18005-18010, June 18, 1999

Signal Relay by Retinoic Acid Receptors  and  in the Retinoic Acid-induced Expression of Insulin-like Growth Factor-binding Protein-3 in Breast Cancer Cells

Yongfeng Shang, Craig R. Baumrucker^§, and Michael H. Green

From the  Nutrition Department and the ^§ Department of Dairy and Animal Science, The Pennsylvania State University, University Park, Pennsylvania 16802

Neither retinoic acid receptor- (RAR) nor insulin-like growth factor-binding protein-3 (IGFBP-3) is expressed in breast cancer cell line MCF-7. The expression of both proteins can be induced in response to all-trans-retinoic acid (atRA). By using an RAR-selective antagonist (Ro 41-5253), we demonstrated that RAR expression was induced by atRA through an RAR-dependent signaling pathway and that RAR induction was correlated with IGFBP-3 induction. However, MCF-7 cells transfected with sense RAR cDNA expressed IGFBP-3 even in the presence of the RAR-selective antagonist Ro 41-5253. On the other hand, antisense RAR cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RAR is directly involved in the mediation of IGFBP-3 induction by atRA. Induction of IGFBP-3 expression by atRA occurs at the transcriptional level, as measured by nuclear run-on assays. Finally, we showed that atRA-induced IGFBP-3 is functionally active in modulating the growth-promoting effect of IGF-I. These experiments indicate that RAR and RAR, both individually and together, are important in mammary gland homeostasis and breast cancer development. By linking IGFBP-3 to RAR, our experiments define the signal intersection between the retinoid and IGF systems in cell growth regulation and explain why loss of RAR might be critical in breast cancer carcinogenesis/progression.

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