SeO(2) induces apoptosis with down-regulation of Bcl-2 and up-regulation of P53 expression in both immortal human hepatic cell line and hepatoma cell line

Mutat Res. 2001 Feb 20;490(2):113-21. doi: 10.1016/s1383-5718(00)00149-2.

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.

Publication types

  • Comparative Study

MeSH terms

  • Apoptosis / drug effects*
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / pathology*
  • Cell Adhesion / drug effects
  • Cell Division / drug effects
  • Cell Line, Transformed / drug effects
  • Cell Line, Transformed / metabolism
  • Gene Expression Regulation / drug effects*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Genes, bcl-2 / drug effects*
  • Genes, p53 / drug effects*
  • Hepatocytes / drug effects*
  • Hepatocytes / metabolism
  • Humans
  • Liver Neoplasms / genetics
  • Liver Neoplasms / pathology*
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
  • Selenium Compounds / pharmacology*
  • Selenium Oxides
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / metabolism
  • Tumor Suppressor Protein p53 / biosynthesis*

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Selenium Compounds
  • Selenium Oxides
  • Tumor Suppressor Protein p53