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Expression of a Dominant-Negative Retinoic Acid Receptor Construct Reduces Retinoic Acid Metabolism and Retinoic Acid-Induced Inhibition of NIH-3T3 Cell Growth

Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892-4255

We have previously reported an unexpected relationship between retinoic acid-induced inhibition of cell growth and the ability of various cell lines to metabolize the retinoid. Here, we report that stable expression of the truncated retinoic acid receptor RAR403, transduced in NIH-3T3 cells by a retroviral vector, rendered the cells resistant to retinoic acid for growth inhibition and reduced their ability to metabolize the retinoid at the same time as it blunted the induction of the target gene transglutaminase II. The data suggest that retinoic acid receptors mediate the growth-inhibitory action of retinoic acid as well as its metabolism and the induction of transglutaminase II.

¹ Present address: Istituto Europeo di Oncologia, Via Ripamonti 435, Milan 20141, Italy.

² To whom requests for reprints should be addressed, at Laboratory of Cellular Carcinogenesis and Tumor Promotion, Building 37 Room 3A-17, 37 Convent Drive, National Cancer Institute, NIH, Bethesda, MD 20892-4255. Phone: (301) 496-2698; Fax: (301) 496-8709; E-mail: luigi_de_luca@Anih.gov.

Received 7/ 1/97. Accepted 8/29/97.

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