[Effects of Arsenic Trioxide on K562 Cell Proliferation and Its Mechanisms]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2016 Dec;24(6):1725-1729. doi: 10.7534/j.issn.1009-2137.2016.06.020.
[Article in Chinese]

Abstract

Objective: To investigate the effects of arsenic trioxide (As2O3) on K562 cell proliferation by regulating cell cycle protein D1 and cyclin-dependent kinase inhibitor p27kip1.

Methods: MTT was used to detect the effect of As2O3 on K562 cell proliferation, so as to screen out the appropriate drug concentration. Furthermore, the K562 cell apoptosis was observed by microscopy. The expression of CyclinD1 and p27kip1 in K562 cells treated with As2O3 was analyzed by reverse transcription-polymerase chain reaction(RT-PCR), immunohistochemistry and Western blot.

Results: As2O3 could inhibit the proliferation of K562 cells in a dose- and time- dependent manner (r= 0.967). And the apoptosis cell number in As2O3 group was significantly higher than that in the control group(P<0.05). As2O3 could markedly inhibit the expression of CyclinD1 in K562 cells(P<0.05), but the expression of P27kip1 was not significantly changed after As2O3 treatment.

Conclusions: As2O3 can induce K562 cell apoptosis and inhibit K562 cell proliferation by regulating the expression of CyclinD1.

MeSH terms

  • Antineoplastic Agents
  • Apoptosis*
  • Arsenic Trioxide
  • Arsenicals
  • Cell Line, Tumor
  • Cell Proliferation*
  • Humans
  • K562 Cells
  • Oxides

Substances

  • Antineoplastic Agents
  • Arsenicals
  • Oxides
  • Arsenic Trioxide