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Papers In Press, published online ahead of print September 4, 2002
Department of Internal Medicine I, University of Ulm, Ulm D-89081
Corresponding Author: roland.schmid{at}medizin.uni-ulm.de
Abstract The immunosuppressive agent cyclosporine affects proliferation depending on the cellular system used. In an attempt to study the inhibitory effect of cyclosporine on proliferation of pancreatic acinar cells we used AR42J cells as a model system. Here we demonstrate that cyclosporine inhibits growth of these cells by inducing G1 cell cycle arrest. This effect is mediated by the 5’ regulatory region of the cyclin D1 gene and leads to a reduction of cyclin D1 mRNA expression and protein abundance. We show that in AR42J cells the proximal cyclin D1 promoter contains a cis regulated element, which is important for the maintenance of basal transcriptional activity. This element overlaps the described cAMP response element (CRE) and confers cyclosporine sensitivity to the cyclin D1 promoter. Furthermore, the DNA-binding activity of the CRE binding protein (CREB) decreases through cyclosporine treatment and this is mediated by cyclosporine-induced reduction of CREB steady-state levels. These results demonstrate that cyclosporine can inhibit proliferation of acinar cells by targeting the cyclin D1 promoter at the proximal CRE via a reduction of CREB protein abundance.
J. Biol. Chem, 10.1074/jbc.M204787200
Submitted on May 16, 2002
Revised on September 4, 2002
Accepted on September 4, 2002
Cyclosporine inhibits growth through the ATF/CREB binding site in the cyclin D1 promoter
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