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Molecular and Cellular Biology, January 1999, p. 889-898, Vol. 19, No. 1
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Cyclosporin A Promotes Translational Silencing of Autocrine Interleukin-3 via Ribosome-Associated Deadenylation

Asha P. K. Nair, Hans H. Hirsch, Marco Colombi, and Christoph Moroni*

Institute for Medical Microbiology, University of Basel, Basel, Switzerland

Received 2 March 1998/Returned for modification 22 May 1998/Accepted 4 September 1998

Translation is regulated predominantly by an interplay between cis elements at the 3' and 5' ends of mRNAs and trans-acting proteins. Cyclosporin A (CsA), a calcineurin antagonist and blocker of interleukin-2 (IL-2) transcription in T cells, was found to inhibit translation of IL-3 mRNA in autocrine mast cell tumor lines. The mechanism involved ribosome-associated poly(A) shortening and required an intact AU-rich element in the 3' untranslated region. FK506, another calcineurin inhibitor, shared the effect. The translational inhibition by CsA was specific to oncogenically induced lymphokines IL-3 and IL-4 but not to IL-6, c-jun, and c-myc, which are expressed in the nonmalignant precursor cells. Furthermore, no translational down-regulation of the mRNA was observed in IL-3-transfected precursor cells. These data suggest that translational silencing is associated with the tumor phenotype.

* Corresponding author. Mailing address: Institute for Medical Microbiology, Petersplatz 10, CH-4003 Basel, Switzerland. Phone: 061-267-31-11. Fax: 061-267-32-98. E-mail: moroni{at}ubaclu.unibas.ch.

Molecular and Cellular Biology, January 1999, p. 889-898, Vol. 19, No. 1
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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