2009Zhonghua zhongyiyao xuekanRequires access

Induction of Apoptosis by Arsenic Trioxide in K562 Cells and its Effect on Bcl-2 and Mutant P53 Proteins

Ying-Xia Tan

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Abstract

Objective:To investigate the apoptosis inducing activity of arsenic trioxide and its effect on the expression of Bcl-2 and mutant P53 proteins.Methods:K562 cells were treated with arsenic trioxide at 1,2,4,8,16μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by DNA ladder and Annexin V/PI fluorescence staining together with flow cytometry.Changes in expression of Bcl-2 and mutant P53 protein was assayed by flow cytometry.Results:MTT tests showed K562 cell proliferation was significantly inhibited by arsenic trioxide in time and dose-dependent fashion.Marked apoptosis was detected by DNA ladder and Annexin V/PI in K562 cells after treatment by arsenic trioxide at 4,8,16μmol/L after 24 hours and increased in a dose-dependent manner.The expression of Bcl-2 and mutant P53 protein decreased in K562 cells induced by arsenic trioxide for 24 hours.Conclusion:Bcl-2 and mutant P53 protein probably correlated with the activation of apoptosis in K562 cells induced by arsenic trioxide.

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Objective:To investigate the apoptosis inducing activity of arsenic trioxide and its effect on the expression of Bcl-2 and mutant P53 proteins.Methods:K562 cells were treated with arsenic trioxide at 1,2,4,8,16μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by DNA ladder and Annexin V/PI fluorescence staining together with flow cytometry.Changes in expression of Bcl-2 and mutant P53 protein was assayed by flow cytometry.Results:MTT tests showed K562 cell proliferation was significantly inhibited by arsenic trioxide in time and dose-dependent fashion.Marked apoptosis was detected by DNA ladder and Annexin V/PI in K562 cells after treatment by arsenic trioxide at 4,8,16μmol/L after 24 hours and increased in a dose-dependent manner.The expression of Bcl-2 and mutant P53 protein decreased in K562 cells induced by arsenic trioxide for 24 hours.Conclusion:Bcl-2 and mutant P53 protein probably correlated with the activation of apoptosis in K562 cells induced by arsenic trioxide.

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Available abstract

Objective:To investigate the apoptosis inducing activity of arsenic trioxide and its effect on the expression of Bcl-2 and mutant P53 proteins.Methods:K562 cells were treated with arsenic trioxide at 1,2,4,8,16μmol/L.Cell growth inhibitory rate was detected by MTT colorimetric assay every 24 hours.Apoptosis rate was analyzed by DNA ladder and Annexin V/PI fluorescence staining together with flow cytometry.Changes in expression of Bcl-2 and mutant P53 protein was assayed by flow cytometry.Results:MTT tests showed K562 cell proliferation was significantly inhibited by arsenic trioxide in time and dose-dependent fashion.Marked apoptosis was detected by DNA ladder and Annexin V/PI in K562 cells after treatment by arsenic trioxide at 4,8,16μmol/L after 24 hours and increased in a dose-dependent manner.The expression of Bcl-2 and mutant P53 protein decreased in K562 cells induced by arsenic trioxide for 24 hours.Conclusion:Bcl-2 and mutant P53 protein probably correlated with the activation of apoptosis in K562 cells induced by arsenic trioxide.

Key concepts: Arsenic trioxide, Apoptosis, Annexin, Flow cytometry, MTT assay, Chemistry, Molecular biology, K562 cells

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