Clinical and Experimental Medicine

, Volume 13, Issue 4, pp 323–328 | Cite as

The heat shock protein 90 inhibitor 17-AAG suppresses growth and induces apoptosis in human cholangiocarcinoma cells

  • Jianjun Zhang
  • Zhichao Zheng
  • Yan Zhao
  • Tao Zhang
  • Xiaohu Gu
  • Wei Yang
Short Communication

Abstract

The aim of this study was to investigate the effects of 17-Allylamino-17-demethoxygeldanamycin (17-AAG), a heat shock protein 90 (HSP90) inhibitor, on the proliferation, cell cycle, and apoptosis of human cholangiocarcinoma (CCA) cells. Cell proliferation and cell cycle distribution were measured by the MTT assay and flow cytometry analysis, respectively. Induction of apoptosis was determined by flow cytometry and Hoechst staining. The expressions of cleaved poly ADP-ribose polymerase (PARP), Bcl-2, Survivin, and Cyclin B1 were detected by Western blot analysis. The activity of caspase-3 was also examined. We found that 17-AAG inhibited cell growth and induced G2/M cell cycle arrest and apoptosis in CCA cells together with the down-regulation of Bcl-2, Survivin and Cyclin B1, and the up-regulation of cleaved PARP. Moreover, increased caspase-3 activity was also observed in CCA cells treated with 17-AAG. In conclusion, our data suggest that the inhibition of HSP90 function by 17-AAG may provide a promising therapeutic strategy for the treatment of human CCA.

Keywords

HSP90 17-AAG Cell cycle arrest Apoptosis Cholangiocarcinoma 

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Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  • Jianjun Zhang
    • 1
  • Zhichao Zheng
    • 1
  • Yan Zhao
    • 1
  • Tao Zhang
    • 1
  • Xiaohu Gu
    • 1
  • Wei Yang
    • 1
  1. 1.The Third Department of SurgeryLiaoning Cancer Hospital and InstituteShenyangPeople’s Republic of China

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