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 RAR alpha403, 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.

Expression of a dominant-negative retinoic acid receptor construct reduces retinoic acid metabolism and retinoic acid-induced inhibition of NIH-3T3 cell growth / M. Isogai, M. V. Chiantore, M. Haque, G. Scita, L. M. De Luca. - In: CANCER RESEARCH. - ISSN 0008-5472. - 57:20(1997 Oct 15), pp. 4460-4-4464.

Expression of a dominant-negative retinoic acid receptor construct reduces retinoic acid metabolism and retinoic acid-induced inhibition of NIH-3T3 cell growth

G. Scita
Penultimo
;
1997

Abstract

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 RAR alpha403, 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.
3T3 Cells; Animals; Recombinant Proteins; Retroviridae; Transglutaminases; Mice; Receptors, Retinoic Acid; Transfection; Genetic Vectors; Kinetics; Tretinoin; Enzyme Induction; Cell Division; Sequence Deletion
Settore MED/04 - Patologia Generale
15-ott-1997
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/199396
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