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Abstract
Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RARα) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. RA lowered RARα transcript and protein, increased RARβ transcripts, and had no effect on RARγ. H-ras transformation downregulated RAR expression and abolished responsiveness to RA. Ha-ras-transformed cells were as active as normal NIH-3T3 cells in RA uptake but were unable to degrade it to medium oxidation products, so that, paradoxically, the resistant cells accumulated 20–30-fold as much RA as the sensitive cells. RA sensitivity/insensitivity correlated with RA metabolism/lack thereof in 15 cell lines in serum-free medium. These data suggest a relationship between RA inhibition of cell growth and intracellular RA metabolism. J. Cell. Physiol. 173:297–300, 1997. Published 1997 Wiley-Liss, Inc.1 This article is a US Government work and, as such, is in the public domain in the United States of America.
Published Version
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