RT Journal Article SR Electronic T1 Antiproliferative Effects of Resveratrol and the Mediating Role of Resveratrol Targeting Protein NQO2 in Androgen Receptor-positive, Hormone-non-responsive CWR22Rv1 Cells JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 3011 OP 3017 VO 29 IS 8 A1 TZE-CHEN HSIEH YR 2009 UL http://ar.iiarjournals.org/content/29/8/3011.abstract AB Trans-resveratrol, a polyphenol present in red wines and various human foods, was first reported to exhibit chemopreventive properties based on studies using a mouse skin cancer model. Our laboratory and others subsequently demonstrated the antiprostate cancer (anti-CaP) activity of resveratrol, as evident in its suppression of cell proliferation, arrest of cell cycle progression, and induction of apoptosis in androgen-responsive LNCaP and androgen-non-responsive DU145 and PC-3 CaP cells. However, the molecular mechanism of action of resveratrol has not been tested in androgen receptor (AR)-positive hormone-non-responsive CWR22Rv1 cells, which mimic the transition stages of prostate carcinoma. In this study, we investigated the antiproliferative effects of resveratrol in the context of modulation of growth suppression and NF-κB expression as mediated by resveratrol targeting protein NQO2, using both control and NQO2 siRNA silenced CWR22Rv1 cells. Exposure to resveratrol resulted in a potent, dose-dependent inhibition of CWR22Rv1 proliferation, which was accompanied by a reduction in the expression of NF-κB p65. The suppression of NF-κB p65 expression was abrogated in NQO2 siRNA silenced CWR22Rv1 cells, suggesting that NQO2 is upstream of and integral to the regulation of NF-κB p65. To our knowledge, this study is the first to reveal that resveratrol targeting protein NQO2 plays a mediating role in resveratrol-induced changes of NF-κB p65, which may contribute to the anti-CaP activities elicited by resveratrol.