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Curr Med Chem. 2013;20(33):4195-202.

In silico and biochemical analyses identify quinone reductase 2 as a target of piceatannol.

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Research Associate Professor, Room 133, Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.


To obtain information on anti-prostate cancer (CaP) activities of piceatannol, a metabolite biotransformed from resveratrol by cytochrome P450 CYP1B, CWR22Rv1 cells were incubated with increasing dose of piceatannol. Proliferation and apoptosis assays in exposed cells showed that piceatannol produced inhibition comparable to resveratrol. To determine whether quinone reductase 2 (NQO2) plays a role in the observed effects, in silico analysis was performed. Piceatannol interacted with NQO2 at the same site as resveratrol forming hydrogen bond with asparagine-161 (ASN161). NQO2 mediated anti-CaP effects of piceatannol were also tested and supported by the attenuation of anti-proliferative activity and reduction in extent of inhibition of NQO2 activity by piceatannol in NQO2-knockdown cells relative to NQO2- expressing cells, and by the copious expression of CYP1B in CWR22Rv1 cells. These results show that NQO2 is an intracellular target for piceatannol, suggesting that CaP prevention by resveratrol may be partially attributed to its conversion to piceatannol.

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