Abstract
Quercetin is a flavonoid present in many vegetables, fruits, and beverages. Due to its anti‐oxidant, anti‐tumor, and anti‐inflammatory activity, quercetin has been studied extensively as a chemoprevention agent in several cancer models. Since most of these studies used higher doses of quercetin than clinically achievable, we focused on the effectiveness of physiologically relevant doses of quercetin. A low dose of quercetin exerted cancer cell‐specific inhibition of proliferation and this inhibition resulted from cell cycle arrest at the G~1~ phase. Quercetin induced p21 CDK inhibitor with a concomitant decrease of phosphorylation of pRb, which inhibits the G~1~/S cell cycle progression by trapping E2F1. A low dose of quercetin induced mild DNA damage and Chk2 activation, which is the main regulator of p21 expression by quercetin. In addition, quercetin down‐regulated the cyclin B1 and CDK1, essential components of G~2~/M cell cycle progression. Inhibition of the recruitment of key transcription factor NF‐Y to cyclin B1 gene promoter by quercetin led to transcriptional inhibition. This study proved that the chemo‐preventive efficacy of a physiologically relevant dose of quercetin can be achievable through the inhibition of cell cycle progression. J. Cell. Biochem. 106: 73–82, 2009. © 2008 Wiley‐Liss, Inc.