Journal
MOLECULAR ENDOCRINOLOGY
Volume 19, Issue 7, Pages 1792-1802Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2004-0445
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Funding
- NCI NIH HHS [CA16672, P50 CA092629, P30 CA016672] Funding Source: Medline
- NIDDK NIH HHS [1R01 DK065156 01, R01 DK065156] Funding Source: Medline
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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 Fas/ FasL-associated death domain protein-like inhibitory protein (c-FLIP) gene, which is a potent inhibitor of Fas/ FasL-mediated apoptosis. The androgen receptor 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. 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 the androgen receptor affects survival and apoptosis of prostate cells through regulation of the c-FLIP gene in response to androgens.
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