Tumour necrosis factor-alpha induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Br J Cancer. 1994 Apr;69(4):627-32. doi: 10.1038/bjc.1994.123.

Abstract

The mechanism by which tumour necrosis factor (TNF)-alpha increases the susceptibility of U87-MG human glioblastoma cells to lysis by natural killer (NK) cells was studied. Treatment with TNF-alpha (100 units ml-1) for 48 h enhanced the susceptibility of tumour cells to lysis by NK cells. Increased susceptibility to lysis was associated with enhanced expression of intercellular adhesion molecule 1 (ICAM-1) and HLA class I antigen. Antisense ICAM-1 oligonucleotide inhibited lysis by NK cells of TNF-alpha-treated tumour cells. In contrast, acid treatment following TNF-alpha treatment increased lysis by NK cells. These findings indicate that TNF-alpha treatment of glioblastoma cells increased their susceptibility to lysis by NK cells, since ICAM-1 up-regulation would have more profound effects on NK susceptibility than would HLA class I antigen up-regulation.

MeSH terms

  • Antigens, Neoplasm / biosynthesis
  • Antigens, Neoplasm / immunology
  • Base Sequence
  • Cell Adhesion Molecules / biosynthesis
  • Cell Adhesion Molecules / immunology
  • Cytotoxicity, Immunologic / drug effects*
  • Fluorescent Antibody Technique
  • Glioblastoma / immunology*
  • Glioblastoma / pathology
  • Histocompatibility Antigens Class I / biosynthesis
  • Histocompatibility Antigens Class I / immunology
  • Humans
  • Intercellular Adhesion Molecule-1
  • Killer Cells, Natural / physiology*
  • Molecular Sequence Data
  • Oligonucleotides, Antisense / metabolism
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / immunology
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation

Substances

  • Antigens, Neoplasm
  • Cell Adhesion Molecules
  • Histocompatibility Antigens Class I
  • Oligonucleotides, Antisense
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1