Get access

Genistein-induced mitotic arrest of gastric cancer cells by downregulating KIF20A, a proteomics study

Authors

  • Guang-Rong Yan,

    1. Institute of Life and Health Engineering, and National Engineering and Research Center for Genetic Medicine, Jinan University, Guangzhou, China
    Search for more papers by this author
    • These authors contributed equally to this study.

  • Fei-Yan Zou,

    1. Institute of Productive Immunology, Jinan University, Guangzhou, China
    Search for more papers by this author
    • These authors contributed equally to this study.

  • Bian-Li Dang,

    1. Institute of Life and Health Engineering, and National Engineering and Research Center for Genetic Medicine, Jinan University, Guangzhou, China
    Search for more papers by this author
  • Ye Zhang,

    1. Institute of Life and Health Engineering, and National Engineering and Research Center for Genetic Medicine, Jinan University, Guangzhou, China
    Search for more papers by this author
  • Guangchuang Yu,

    1. Institute of Life and Health Engineering, and National Engineering and Research Center for Genetic Medicine, Jinan University, Guangzhou, China
    Search for more papers by this author
  • Xiao Liu,

    1. Institute of Productive Immunology, Jinan University, Guangzhou, China
    Search for more papers by this author
  • Qing-Yu He

    Corresponding author
    • Institute of Life and Health Engineering, and National Engineering and Research Center for Genetic Medicine, Jinan University, Guangzhou, China
    Search for more papers by this author

  • Colour Online: See the article online to view Figs. 1–3 in colour.

Correspondence: Dr. Guang-Rong Yan, Institute of Life and Health Engineering, Jinan University, Guangzhou 510632, China

E-mail: tgryan@jnu.edu.cn

Fax: +86-20-85224372

Additional corresponding author: Professor Qing-Yu He, E-mail: tqyhe@jnu.edu.cn

Abstract

Genistein exerts its anticarcinogenic effects by inducing G2/M arrest and apoptosis of cancer cells. However, the precise molecular mechanism of action of genistein has not been completely elucidated. In this study, we used quantitative proteomics to identify the genistein-induced protein alterations in gastric cancer cells and investigate the molecular mechanism responsible for the anti-cancer actions of genistein. Total 86 proteins were identified to be regulated by genistein, most of which were clustered into the regulation of cell division and G2/M transition, consistent with the anti-cancer effect of genistein. Many proteins including kinesin family proteins, TPX2, CDCA8, and CIT were identified for the first time to be regulated by genistein. Interestingly, five kinesin family proteins including KIF11, KIF20A, KIF22, KIF23, and CENPF were found to be simultaneously downregulated by genistein. Significantly decreased KIF20A was selected for further functional studies. The silencing of KIF20A inhibited cell viability and induced G2/M arrest, similar to the effects of genistein treatment in gastric cancer. And the silencing of KIF20A also increased cancer cell sensitivity to genistein inhibition, whereas overexpression of KIF20A markedly attenuated genistein-induced cell viability inhibition and G2/M arrest. These observations suggested that KIF20A played an important role in anti-cancer actions of genistein, and thus may be a potential molecular target for drug intervention of gastric cancer.

Get access to the full text of this article

Ancillary