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Retinoic Acid Inhibition of Serum-induced c-fos Transcription in a Fibrosarcoma Cell Line¹

Departments of Microbiology [P. J., T-s. C.] and Human Biological Chemistry and Genetics [L-N. L. C., J. S.], University of Texas Medical Branch, Galveston, Texas 77550, and Institut für Virologie and Immunologie, Würzburg, Germany [J. S-S.]

We investigated the mechanism by which retinoic acid causes growth arrest and flat reversion of SSV-NRK, simian sarcoma virus-transformed normal rat kidney cells. Northern analysis revealed that both chronic (7 days) and acute (6 h) retinoic acid treatment of serum-stimulated SSV-NRK cells caused a 6-fold decrease in c-fos mRNA levels. In addition, nuclear run-on experiments showed that retinoic acid regulated c-fos expression in SSV-NRK cells at the transcriptional initiation level. Attenuation of c-fos transcription was equal in both retinoic acid-treated and control cells, and no increased c-fos mRNA turnover was detected in retinoic acid-treated cells. Furthermore, there was no observed change in the c-fos mRNA levels after only 30 min of retinoic acid treatment, suggesting that a mechanism involving the interruption of the signal transduction mechanism at the membrane level is unlikely. Because it has been shown that c-fos expression plays a pivotal role in mitogenesis of quiescent fibroblasts, we conclude that the retinoic acid-mediated down-regulation of c-fos expression is a mechanism for growth inhibition in SSV-NRK cells.

¹ This work was supported by USPHS Grant ES04132 to L-N. L. C. and USPHS Grant GM27589 to T-s. C. P. J. is the recipient of a McLaughlin postdoctoral fellowship.

² To whom requests for reprints should be addressed, at the Department of Microbiology, University of Texas Medical Branch, Galveston, TX 77550.

Received 9/27/91. Accepted 2/20/92.

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