Abstract
Androgens via their receptor (AR) may play a role in prostate cancer etiology. This study focuses on the inhibitory effects of resveratrol on androgen action in the LNCaP prostate cancer cell line. We found that resveratrol represses different classes of androgen up-regulated genes at the protein or mRNA level including prostate-specific antigen, human glandular kallikrein-2, AR-specific coactivator ARA70, and the cyclin-dependent kinase inhibitor p21. This inhibition is likely attributable to a reduction in AR contents at the transcription level, inhibiting androgen-stimulated cell growth and gene expression. This study suggests that resveratrol may be a useful chemopreventive/chemotherapeutic agent for prostate cancer.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Antineoplastic Agents, Phytogenic / pharmacology*
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins / genetics
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Enzyme Inhibitors / metabolism
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Gene Expression Regulation, Neoplastic / drug effects*
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Humans
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Male
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Nuclear Receptor Coactivators
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Oncogene Proteins*
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Prostate-Specific Antigen / genetics
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Prostatic Neoplasms
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RNA, Messenger / genetics
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Receptors, Androgen / drug effects
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Receptors, Androgen / genetics
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Receptors, Androgen / physiology*
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Resveratrol
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Stilbenes / pharmacology*
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Tissue Kallikreins / genetics
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Trans-Activators / genetics
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Transcription Factors*
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Transcription, Genetic / drug effects
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Tumor Cells, Cultured
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Up-Regulation / drug effects
Substances
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Antineoplastic Agents, Phytogenic
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CDKN1A protein, human
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins
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Enzyme Inhibitors
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NCOA4 protein, human
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Nuclear Receptor Coactivators
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Oncogene Proteins
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RNA, Messenger
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Receptors, Androgen
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Stilbenes
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Trans-Activators
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Transcription Factors
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Tissue Kallikreins
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Prostate-Specific Antigen
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Resveratrol