Journal of Chinese Pharmaceutical Sciences ›› 2017, Vol. 26 ›› Issue (6): 432-439.DOI: 10.5246/jcps.2017.06.047

• Original articles • Previous Articles     Next Articles

Vanadium compounds induce stronger growth suppression in PTEN-deficient prostate cancer cells by ROS-mediated mechanism

Yihua Hong, Tongtong Liu, Yanjun Liu, Jingxuan Wu, Xiaogai Yang*   

  1. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
  • Received:2017-04-28 Revised:2017-05-03 Online:2017-06-29 Published:2017-05-28
  • Contact: Tel.: +86-010-82805956, E-mail:
  • Supported by:
    National Natural Science Foundation of China (Grant No. 21171011 and 21671009).


In the present study, we investigated the antiproliferative effect and the underlying mechanism of three antidiabetic vanadium compounds, metavanadate, VO(acac)2 and VO(ma)2, in human prostate cancer cells (PC-3 and DU-145). The results showed that vanadium compounds caused cell cycle arrest at G2/M phase evidenced by the elevation of phosphorylated Cdc2 at tyr-15. Moreover, the results revealed that vanadium compounds induced reactive oxygen species (ROS) elevation in the two cell lines. The decreased level of Cdc25C could be rescued by the antioxidant, N-acetylcysteine, indicating that vanadium compounds-induced G2/M arrest was mediated by ROS. Additionally, the three vanadium compounds exerted more potent growth inhibitory effect on PC-3 cells which are PTEN-deficient and with higher level of basal ROS. It suggested that PTEN protein might serve as a biomarker for the selectivity of antitumor therapy using ROS-generating agents. Since the studied vanadium compounds have been shown the antidiabetic activities in the previous studies, there may be additional benefits in the potential application of vanadium compounds to suppress the growth of prostate cancer cells. 

Key words: Vanadium compounds, Reactive oxygen species, PTEN, Prostate cancer, Diabetes

CLC Number: