2006•Unpublished venueRequires access

The study of antitumor mechanism of sodium arsenite on gastric carcinoma cell line SGC-7901 in vitro

Tang Wei-xu

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Abstract

Objective To investigate the antitumor mechanism of sodium arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MTT assay, light microscopy, electron microscopy, flow cytometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic behavior of SGC-7901 cells. Results Sodium arsenite (2.50 ~ 40.00 μmol/L) could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration(IC50) was 8.69 μmol/L after 72 hours' treatment. SGC-7901 cells were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 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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Objective To investigate the antitumor mechanism of sodium arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MTT assay, light microscopy, electron microscopy, flow cytometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic behavior of SGC-7901 cells. Results Sodium arsenite (2.50 ~ 40.00 μmol/L) could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration(IC50) was 8.69 μmol/L after 72 hours' treatment. SGC-7901 cells were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 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 arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MTT assay, light microscopy, electron microscopy, flow cytometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic behavior of SGC-7901 cells. Results Sodium arsenite (2.50 ~ 40.00 μmol/L) could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration(IC50) was 8.69 μmol/L after 72 hours' treatment. SGC-7901 cells were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 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, Arsenite, Cell culture, Chemistry, In vitro, Molecular biology, Flow cytometry

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