[Inhibitory effect of apatinib on HL-60 cell proliferation and its mechanism]

Nan Fang Yi Ke Da Xue Xue Bao. 2011 May;31(5):871-4.
[Article in Chinese]

Abstract

Objective: To investigate the effect of apatinib, a small-molecule vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor, on the proliferation of human acute myeloid leukemia HL-60 cells and explore the possible mechanism.

Methods: MTT assay was used to assess the cytotoxicity of apatinib in HL-60 cells. The apoptosis and cell cycle changes of the cells in response to apatinib treatment were analyzed by flow cytometry, and Western blotting was used to assay P-Akt and P-Erk1/2 expressions in the cells.

Results: Apatinib significantly inhibited the proliferation of HL-60 cells in vitro with an IC(50) of 4.96∓0.32 µmol/L. Apatinib treatment significantly increased the apoptotic rate of the cells in a dose-dependent manner, but produced no significant effect on the cell cycle (P>0.05). Western blotting showed that the expressions of P-Akt and P-Erk1/2 decreased in HL-60 cells after a 48-h apatinib treatment.

Conclusion: Apatinib inhibits the proliferation of HL-60 cells by inducing cell apoptosis probably through the mechanism of inhibiting the expressions of the Akt/Erk1/2 signal transduction pathway.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Apoptosis / drug effects*
  • Cell Proliferation / drug effects*
  • HL-60 Cells
  • Humans
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Pyridines / chemistry
  • Pyridines / pharmacology*

Substances

  • Pyridines
  • apatinib
  • Protein-Tyrosine Kinases