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Induction of apoptosis and inhibition of NF‐κB activation in human prostate cancer cells by the cis ‐9, trans ‐11 but not the trans ‐10, cis‐ 12 isomer of conjugated linoleic acid
Author(s) -
Song HyunJu,
Sneddon Alan A.,
Heys Steven D.,
Wahle Klaus W.J.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20351
Subject(s) - apoptosis , lncap , annexin , flow cytometry , phosphorylation , cancer research , prostate cancer , microbiology and biotechnology , tumor necrosis factor alpha , biology , endocrinology , medicine , cancer , biochemistry
Abstract BACKGROUND Conjugated linoleic acids (CLAs) have anti‐tumorigenic properties in animal models and anti‐proliferative effects on cancer cells in vitro. Previous studies have shown that the NF‐κB pathway is involved regulating anti‐apoptotic gene expression. The present study investigated the effects of CLAs ( cis ‐9, trans ‐11, and trans ‐10, cis ‐12 isomers and a 50:50 mixture) on apoptosis and NF‐κB activation in LNCaP cells. METHODS Apoptosis was assessed by annexin V staining using flow cytometry. TNF‐α‐induced NF‐κB activity was determined by gel shift and reporter gene assays in addition to monitoring IκBα phosphorylation. RESULTS Only the CLA cis ‐9, trans ‐11 isomer significantly increased TNF‐α‐induced apoptosis (by 59%), which correlated with a reduction in NF‐κB transcriptional activity (by 35%, P < 0.05), NF‐κB binding activity (by 15%, P < 0.05), and phosphorylation of IκBα (by 36%, P < 0.01). CONCLUSIONS Our results may offer a mechanistic explanation for the reported inhibition of prostate tumor growth by CLAs in animal models of disease. Prostate © 2006 Wiley‐Liss, Inc.