Arsenic trioxide inducing G_2/M cell cycle arrest and the expression of Survivin in chronic myeloid leukemic cells
Zhongping Liu
Abstract
Zhongping Liu
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.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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