2004Journal of Clinical Internal MedicineRequires access

Arsenic trioxide inducing G_2/M cell cycle arrest and the expression of Survivin in chronic myeloid leukemic cells

Zhongping Liu

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Abstract

Objective To explore the characteristic and m ec hanism of arsenic trioxide (As 2O 3) on chronic myeloid leukemic cells (K562).Methods After K562 cells were treated with As 2O 3 of various concentrations,cell proliferation was tested by MTT assay,the distribution of c ell cycles,cell apoptosis and the expression of Survivin antigen were detected b y flow cytometry,and the content of expression of survivin gene was determined b y RT-PCR.Results As 2O 3(2~10μmol/L) inhibited K562 cells growth eff ectively,but could not induce significant cell apoptosis.The percentage of K562 cells at G 2/M phase increased,and the expression of Survivin mRNA and protein was up-regulated after the treatment.Conclusion As 2O 3 inhibited the growth of K562 cells by indu cing them arrest at G 2/M cell cycle.The up-regulation of Survivin expression might be one of the possible mechanisms of their resistance to As 2O 3 inducin g cell apoptosis.

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Objective To explore the characteristic and m ec hanism of arsenic trioxide (As 2O 3) on chronic myeloid leukemic cells (K562).Methods After K562 cells were treated with As 2O 3 of various concentrations,cell proliferation was tested by MTT assay,the distribution of c ell cycles,cell apoptosis and the expression of Survivin antigen were detected b y flow cytometry,and the content of expression of survivin gene was determined b y RT-PCR.Results As 2O 3(2~10μmol/L) inhibited K562 cells growth eff ectively,but could not induce significant cell apoptosis.The percentage of K562 cells at G 2/M phase increased,and the expression of Survivin mRNA and protein was up-regulated after the treatment.Conclusion As 2O 3 inhibited the growth of K562 cells by indu cing them arrest at G 2/M cell cycle.The up-regulation of Survivin expression might be one of the possible mechanisms of their resistance to As 2O 3 inducin g cell apoptosis.

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Available abstract

Objective To explore the characteristic and m ec hanism of arsenic trioxide (As 2O 3) on chronic myeloid leukemic cells (K562).Methods After K562 cells were treated with As 2O 3 of various concentrations,cell proliferation was tested by MTT assay,the distribution of c ell cycles,cell apoptosis and the expression of Survivin antigen were detected b y flow cytometry,and the content of expression of survivin gene was determined b y RT-PCR.Results As 2O 3(2~10μmol/L) inhibited K562 cells growth eff ectively,but could not induce significant cell apoptosis.The percentage of K562 cells at G 2/M phase increased,and the expression of Survivin mRNA and protein was up-regulated after the treatment.Conclusion As 2O 3 inhibited the growth of K562 cells by indu cing them arrest at G 2/M cell cycle.The up-regulation of Survivin expression might be one of the possible mechanisms of their resistance to As 2O 3 inducin g cell apoptosis.

Key concepts: Survivin, Arsenic trioxide, Apoptosis, K562 cells, Flow cytometry, Cell cycle, Molecular biology, Myeloid leukemia

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