<p>Anthocyanins are a group of plant secondary metabolites belonging to the polyphenol family. They are beneficial bioactive compounds for numerous health problems, without side effects. Although anthocyanins have been reported to possess anti-cancer activity, studies of their effects on prostate cancer cells remain insufficient. In this study, the mechanism of the anti-cancer activity of anthocyanins extracted from the fruit of <i>Vitis coignetiae</i> Pulliat in human prostate carcinoma (PCa) cells was investigated. The results of this study indicate that anthocyanins-induced suppression of PCa cell proliferation is associated with G1 phase cell cycle arrest, along with the induction of cyclin-dependent kinase (Cdk) inhibitor p21^WAF1/CIP1 expression, suppression of cyclin D1 and E expression, and dephosphorylation of retinoblastoma protein (pRB). In addition, anthocyanins markedly enhanced the complex formation between p21^WAF1/CIP1 and Cdks, as well as pRB and the transcription factor E2Fs, respectively. Anthocyanins also induced apoptosis by induction of the expression of death receptor-related proteins and activation of caspases. Moreover, anthocyanins interfered with mitochondrial integration by altering the level of Bcl-2 family proteins to increase cytoplasmic release of cytochrome <i>c</i>, suggesting that activation of both the intrinsic and extrinsic pathways contributed to anthocyanin-induced apoptosis. Furthermore, anthocyanins significantly enhanced the generation of reactive oxygen species (ROS), whereas ROS scavenger restored reduced viability by attenuating anthocyanins-mediated growth arrest and apoptosis. Collectively, the present findings demonstrate that the antiproliferative efficacy of anthocyanins in PCa cells can be achieved through ROS-dependent pathway. </p>