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
Keywords: Resveratrol, piceatannol, biotransformation, chemoprevention, cytochrome P450 CYP1B1, CWR22Rv1 prostate
cancer cells, in silico analysis, NQO2, NQO2 knockdown.
Rights & PermissionsPrintExport