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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
15
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pubmed:dateCreated |
2008-9-22
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pubmed:abstractText |
Prostate tumors initially regress in response to androgen-ablation therapy. However, most cancers eventually relapse with an androgen-depletion-independent (ADI) phenotype that is often more aggressive than the original androgen-dependent (AD) tumor. Importantly, most relapsed tumors still rely upon androgen receptor (AR) activity for proliferation and survival. The cellular Fas/FasL-associated death domain protein-like inhibitory protein (FLIP) inhibits activation of procaspase-8 by death receptor-mediated signaling at the cell surface. In the current study, we examined the androgenic regulation of FLIP and its contribution to protecting prostate cancer cells from death receptor-mediated apoptosis.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-11278284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-11593415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-11861374,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-12811833,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-12890564,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-14689583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15013685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15389811,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15466204,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15470210,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15643172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15701649,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15731171,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-15833082,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-16518832,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-16541419,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-17237035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-17907960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-2440339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-9211860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-9217161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18726983-9661880
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1097-0045
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pubmed:author |
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pubmed:copyrightInfo |
(c) 2008 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1696-706
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pubmed:dateRevised |
2011-5-12
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pubmed:meshHeading |
pubmed-meshheading:18726983-Androgens,
pubmed-meshheading:18726983-Animals,
pubmed-meshheading:18726983-Apoptosis,
pubmed-meshheading:18726983-CASP8 and FADD-Like Apoptosis Regulating Protein,
pubmed-meshheading:18726983-Cell Line, Tumor,
pubmed-meshheading:18726983-Cytoprotection,
pubmed-meshheading:18726983-Male,
pubmed-meshheading:18726983-Orchiectomy,
pubmed-meshheading:18726983-Prostate,
pubmed-meshheading:18726983-Prostatic Neoplasms,
pubmed-meshheading:18726983-RNA, Messenger,
pubmed-meshheading:18726983-RNA, Small Interfering,
pubmed-meshheading:18726983-Rats,
pubmed-meshheading:18726983-Rats, Wistar,
pubmed-meshheading:18726983-Receptors, Androgen,
pubmed-meshheading:18726983-Seminal Vesicles,
pubmed-meshheading:18726983-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:18726983-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Induction of FLIP expression by androgens protects prostate cancer cells from TRAIL-mediated apoptosis.
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pubmed:affiliation |
Department of Urology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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