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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2004, Vol. 9 ›› Issue (5): 569-572.

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Arsenic trioxide-induced apoptosis in K562/ADM cells and its mechanisms

WANG Dong-Hai, WEI Hu-Lai1, SU Yong-Hong, HAO Chun-Yan2, LIU Jian-Min1   

  1. Department of Hematology, the First Affiliated Hospital, 1Laboratory Center for Medical Science, 2Department of Biochemistry and Molecular Biology, Lanzhou Medical College, Lanzhou 730000, Gansu, China
  • Received:2004-02-06 Revised:2004-03-08 Published:2020-11-22

Abstract: AIM: To observe the apoptosis of K562/ ADM cells induced by As2O3 and to explore its possible mechanisms. METHODS: MTT assay, Wright-Giemsa staining, DNA agarose gel electrophoresis and cell cycle analysis were used to examine apoptosis in K562/ADM cells.Expression levels of Fas, Bcl-2 and P53 antigens were measured with FCM.Colorimetric assay was employed to detect the activation of Caspase3. RESULTS: As2O3 inhibited growth of K562/ADM cells.Morphological changes typical of apoptosis were observed through light microscopy.Agarose gel electrophoresis showed evident DNA fragmentation.Cell cycle analysis indicated increased Sub-G1 proportion and apoptosis rate, as well as apparent G2 M phase arrest.The expression of Fas and P53 antigens significantly increased after application of As2O3.Caspase 3 was also activated by As2O3. CONCLUSION: As2O3 induces apoptosis in K562/ADM cells by activating Caspase 3 via a Fas-dependent pathway.

Key words: leukemia, multidrug resistance, arsenic trioxide, apoptosis

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