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Submitted on November 3, 2004
Accepted on February 14, 2005
Department of Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030; Department of Pathology, New York University School of Medicine and New York Harbor Healthcare System, New York, NY 10010; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021
* To whom correspondence should be addressed. E-mail: zhenwang{at}mdanderson.org.
Androgens provide survival signals to prostate epithelial cells, and androgen ablation induces apoptosis in the prostate gland. However, the molecular mechanisms of actions of the androgen-signaling pathway in these processes are not fully understood. Here, we report that androgens induced expression of the cellular FLIP (c-FLIP) gene, which is a potent inhibitor of Fas/FasL-mediated apoptosis. The androgen receptor (AR) was recruited to the promoter of the c-FLIP gene in the presence of androgens. We found that c-FLIP promoter contained multiple functional androgen response elements (AREs). In addition, we show that c-FLIP overexpression accelerated progression to androgen independence by inhibiting apoptosis in LNCaP prostate tumors implanted in nude mice. Our results suggest that AR affects survival and apoptosis of prostate cells through regulation of the c-FLIP gene in response to androgens.
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