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Role of reactive oxygen species in the antiproliferative effects of metavanadate on human prostate cancer DU145 cells

Tong-Tong Liu, Yan-Jun Liu, Xiao-Gai Yang*   

  1. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191
  • Received:2011-05-30 Revised:2011-10-10 Online:2012-01-01 Published:2012-01-01
  • Contact: Xiao-Gai Yang*

Abstract:

In the present study, the effects of metavanadate on the human prostate cancer cell line DU145 and the underlying mechanism were investigated. The results showed that metavanadate can cause cell cycle arrest at G2/M phase which was evidenced by cell cycle analysis and the increased phosphorylation of Cdc2 at its inactive Tyr-15 site. In addition, the results showed that metavanadate can induce reactive oxygen species (ROS) elevation and decrease the level of Cdc25C. This process can be rescued by an antioxidant, N-acetyl cysteine. In conclusion, the results demonstrate that metavanadate can inhibit cell proliferation via cell cycle arrest at G2/M phase in DU145 cells. Metavanadate-induced ROS formation may play an important role in this process by mediating the degradation of Cdc25C.

Key words: Metavanadate, G2/M cell cycle arrest, Cdc25C, Reactive oxygen species

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