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Arsenic trioxide inhibits proliferation in K562 cells by changing cell cycle and survivin expression

Xiaofei Wu1, Zhichao Chen, Zhongping Liu

  • 1Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban
|December 14, 2004
PubMed

Insights

Arsenic trioxide inhibits chronic myeloid leukemia (K562) cell growth by arresting the cell cycle at the G2/M phase. Increased Survivin expression may contribute to K562 cells resistance to arsenic trioxide-induced apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm.
  • Arsenic trioxide (As2O3) is a chemotherapeutic agent with demonstrated efficacy in certain leukemias.
  • Survivin is an inhibitor of apoptosis protein (IAP) implicated in cancer cell survival and drug resistance.

Purpose of the Study:

  • To elucidate the mechanisms by which As2O3 inhibits K562 cell proliferation.
  • To investigate the role of Survivin in As2O3-induced apoptosis in K562 cells.

Main Methods:

  • K562 cells were treated with varying concentrations of As2O3.
  • Cell proliferation was assessed using MTT assay.
  • Cell cycle distribution and apoptosis were analyzed by flow cytometry.
  • Survivin protein and mRNA expression were quantified via flow cytometry and RT-PCR, respectively.

Main Results:

  • As2O3 (2-10 micromol/L) significantly inhibited K562 cell growth without inducing substantial apoptosis.
  • A dose-dependent increase in G2/M phase cell cycle arrest was observed with As2O3 treatment.
  • Survivin mRNA and protein expression were upregulated in response to As2O3 exposure.

Conclusions:

  • As2O3 inhibits K562 cell proliferation primarily through G2/M phase cell cycle arrest.
  • Upregulation of Survivin may confer resistance to As2O3-induced apoptosis in K562 cells, suggesting a potential therapeutic target.

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