Tumor necrosis factor-alpha gene transfer augments anti-Fas antibody-mediated apoptosis in human glioma cells

Jpn J Cancer Res. 1996 May;87(5):543-7. doi: 10.1111/j.1349-7006.1996.tb00257.x.

Abstract

To effectively induce apoptosis in human glioma cells, we tried to transfer the tumor necrosis factor (TNF)-alpha gene into glioma cells to produce TNF-alpha locally in these cells. The stable transfectants of three glioma cells (U251-SP, U251-MG, and T98G) were resistant to exogenous TNF-alpha, but their cell surface expression of the Fas antigen was dramatically enhanced by about 10 to 100-fold as compared with untransfected glioma cells exposed to exogenous TNF-alpha. The Fas antigen is a transmembrane cytokine receptor protein of the nerve growth factor/TNF receptor superfamily. Although the untransfected glioma cells tested were resistant to anti-Fas antibody-mediated apoptosis, the TNF-alpha gene-transfected glioma cells exhibited high susceptibility to anti-Fas antibody-mediated apoptosis. Thus, TNF-alpha gene transfer combined with anti-Fas antibodies may be useful for the treatment of malignant glioma.

MeSH terms

  • Antibodies / therapeutic use*
  • Apoptosis*
  • Brain Neoplasms / immunology
  • Brain Neoplasms / pathology
  • Brain Neoplasms / therapy*
  • Gene Transfer Techniques*
  • Glioma / immunology
  • Glioma / pathology
  • Glioma / therapy*
  • Humans
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / therapeutic use*
  • fas Receptor / immunology*
  • fas Receptor / metabolism

Substances

  • Antibodies
  • Tumor Necrosis Factor-alpha
  • fas Receptor