Abstract
An immortal human hepatic cell line HL-7702 and human hepatoma cell line SMMC-7721 were treated with 3-30 microM SeO(2). SeO(2) at 30 microM markedly inhibited cell proliferation and viability, and prompted apoptosis of both normal hepatic and hepatoma cells after 48h treatment. SeO(2) could also down-regulate the Bcl-2 level, greatly in HL-7702 and slightly in SMMC-7721 cells, but up-regulate wild type P53 level a little in HL-7702 and significantly in SMMC-7721 cells. The Bcl-2/P53 value was closely correlated with the apoptotic rate as well as SeO(2) concentrations.
MeSH terms
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Apoptosis / drug effects*
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / pathology*
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Cell Adhesion / drug effects
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Cell Division / drug effects
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Cell Line, Transformed / drug effects
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Cell Line, Transformed / metabolism
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Gene Expression Regulation / drug effects*
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Gene Expression Regulation, Neoplastic / drug effects
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Genes, bcl-2 / drug effects*
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Genes, p53 / drug effects*
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Hepatocytes / drug effects*
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Hepatocytes / metabolism
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Humans
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Liver Neoplasms / genetics
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Liver Neoplasms / pathology*
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
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Selenium Compounds / pharmacology*
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Selenium Oxides
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Tumor Cells, Cultured / drug effects
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Tumor Cells, Cultured / metabolism
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Tumor Suppressor Protein p53 / biosynthesis*
Substances
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Proto-Oncogene Proteins c-bcl-2
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Selenium Compounds
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Selenium Oxides
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Tumor Suppressor Protein p53