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Papers In Press, published online ahead of print August 10, 2005
Pathology Dept., USF College of Medicine, Tampa, FL 33612-4799
Corresponding Author: wbai{at}hsc.usf.edu
Recent studies suggest that growth inhibition by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] represents an innovative approach to ovarian cancer (OCa) therapy. To understand the molecular mechanism of 1,25(OH)2D3 action, we profiled the hormone induced changes in the transcriptome of OCa cells using microarray technology. More than two hundred genes were identified to be regulated by 1,25(OH)2D3. RT-PCR analyses confirmed the regulation of a group of apoptosis-related genes, including the up-regulation of decoy receptor that inhibits TRAIL action, TRAIL receptor 4 (TRAIL-R4), and the down-regulation of Fas, the receptor that mediates the action of Fas ligand. The regulation was further confirmed at the protein level. Consistent with the regulation of the death receptors, pre-treatment with 1,25(OH)2D3 decreased apoptosis induced by TRAIL and Fas ligand. Because persistent 1,25(OH)2D3 treatment has been shown to induce apoptosis in OCa, the hormone appears to exert a dual effect on the death of OCa cells. Knock down of TRAIL-R4 by RNA interference or ectopic expression of Fas relieved the suppressive effect of 1,25(OH)2D3, showing that molecular manipulation of death receptors is a viable approach to overcome the protective effect of 1,25(OH)2D3 on the apoptosis of OCa. These strategies may allow OCa patients to benefit from therapy with both 1,25(OH)2D3 and ligands for death receptors, such as TRAIL, shown to selectively induce apoptosis in cancer but not normal cells.
J. Biol. Chem, 10.1074/jbc.M506648200
Submitted on June 20, 2005
Revised on July 27, 2005
Accepted on August 10, 2005
Suppression of death receptor-mediated apoptosis by 1,25-dihydroxyvitamin D3 revealed by microarray analysis
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