[Proliferation and Apoptosis of Leukemia Cell Line K562 Treated with HSP90 Inhibitor 17-DMAG]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2017 Aug;25(4):998-1002. doi: 10.7534/j.issn.1009-2137.2017.04.007.
[Article in Chinese]

Abstract

Objective: To investigate the role of HSP90 in proliferation and apoptosis of leukemia cells K562 through detecting the effect of HSP90 inhibitors 17-[2-(Dimethylamino) ethyl] amino-17-desmethoxygeldanamycin(17-DMAG) on leukemia K562 cell lines.

Methods: The K562 cells were treated with HSP90 inhibitors 17-DMAG, the semi-quantitative PCR was used to detect HSP90 gene expression, the WST was used to detect the effect 17-DMAG on cell proliferation as well as Annexin V flow cytometry was used to detect the cell apoptosis.

Results: After 17-DMAG treated the K562 cells in different stage, the K562 cell growth was obviously inhibited with time dependent (48 h)(r=0.9918) and dose dependent(3.2 µmol/L) manners (r=0.9999) (P<0.01); after the K562 cells in different stage were treated with different concentrations of 17-DMAG, the K562 cells showed significant apoptosis and with dosage-dependent mauner (r=0.9903)(P<0.01); HSP90 mRNA expression decreased significantly after K562 cells were treated with different concentrations of 17-DMAG for 48 hours. 17-DAMG down-regulated the HSP90 mRNA expression in dosage-dependent mauner as well(r=0.9227) (P<0.01).

Conclusion: HSP90 inhibitor 17-DMAG can inhibit the proliferation of K562 cells and induce their apoptosis. This study result provides laboratory basis for the treatment of leukemia patients with 17-DMAG.

MeSH terms

  • Apoptosis*
  • Benzoquinones
  • Cell Proliferation*
  • HSP90 Heat-Shock Proteins
  • Humans
  • K562 Cells
  • Lactams, Macrocyclic
  • Leukemia

Substances

  • Benzoquinones
  • HSP90 Heat-Shock Proteins
  • Lactams, Macrocyclic
  • 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin