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Antitumor Mechanism of Sodium Arsenic on Human Gastric Carcinoma Cell Line BGC-823 in Vitro

Wentao Zhao, Yanqing Wang, Weixue Tang

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Abstract

Objective To investigate the antitumor mechanism of sodium arsenic on human gastric carcinoma cell line BGC-823 in vitro.Methods MTT assay, light microscopy,electron microscopy,flow cytometry,and immunocytochemical staining were used to detect the effect of sodium arsenic on biologic behavior of BGC-823 cells.Results Sodium arsenic inhibited the growth of BGC-823 cells in a time and concentration dependent fashion,its 50% inhibitory concentration(IC_ 50 ) was 4.86μmol/L.BGC-823 cells were arrested significantly in G_ 2 /M phase when treated with sodium arsenic. BGC-823 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenic.Sodium arsenic up-regulated Caspase-3 protein expression in BGC-823 cells.Conclusion Sodium arsenite could obviously inhibit the proliferation of BGC-823 cells:induce cell cycle arrest and apoptosis and necrosis of the cells.Its mechanism is possibly associated with inhibition of elimination of ROS, and the up-regulated expression of Caspase-3 protein.

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What this paper is about

Objective To investigate the antitumor mechanism of sodium arsenic on human gastric carcinoma cell line BGC-823 in vitro.Methods MTT assay, light microscopy,electron microscopy,flow cytometry,and immunocytochemical staining were used to detect the effect of sodium arsenic on biologic behavior of BGC-823 cells.Results Sodium arsenic inhibited the growth of BGC-823 cells in a time and concentration dependent fashion,its 50% inhibitory concentration(IC_ 50 ) was 4.86μmol/L.BGC-823 cells were arrested significantly in G_ 2 /M phase when treated with sodium arsenic. BGC-823 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenic.Sodium arsenic up-regulated Caspase-3 protein expression in BGC-823 cells.Conclusion Sodium arsenite could obviously inhibit the proliferation of BGC-823 cells:induce cell cycle arrest and apoptosis and necrosis of the cells.Its mechanism is possibly associated with inhibition of elimination of ROS, and the up-regulated expression of Caspase-3 protein.

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Available abstract

Objective To investigate the antitumor mechanism of sodium arsenic on human gastric carcinoma cell line BGC-823 in vitro.Methods MTT assay, light microscopy,electron microscopy,flow cytometry,and immunocytochemical staining were used to detect the effect of sodium arsenic on biologic behavior of BGC-823 cells.Results Sodium arsenic inhibited the growth of BGC-823 cells in a time and concentration dependent fashion,its 50% inhibitory concentration(IC_ 50 ) was 4.86μmol/L.BGC-823 cells were arrested significantly in G_ 2 /M phase when treated with sodium arsenic. BGC-823 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenic.Sodium arsenic up-regulated Caspase-3 protein expression in BGC-823 cells.Conclusion Sodium arsenite could obviously inhibit the proliferation of BGC-823 cells:induce cell cycle arrest and apoptosis and necrosis of the cells.Its mechanism is possibly associated with inhibition of elimination of ROS, and the up-regulated expression of Caspase-3 protein.

Key concepts: Sodium arsenite, Apoptosis, Chemistry, Cell culture, Flow cytometry, Arsenic, Sodium, In vitro

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