Facilitation of H2O2-induced A172 human glioblastoma cell death by insertion of oxidative stress-sensitive TRPM2 channels

Anticancer Res. 2007 Nov-Dec;27(6B):3987-92.

Abstract

The melastatin-like transient receptor potential M2 (TRPM2) channel is a Ca2+ permeable channel that is activated by reactive oxygen species (ROS), and its activation induces necrotic cell death. The effect of insertion of TRPM2 into A172 human glioblastoma cells (A172 cells) was investigated. The insertion of TRPM2 channels enhanced cell death induced by H2O2 in the A172 cells. An H2O2-induced Ca2+ increase was observed in TRPM2-expressing cells, but not in wild-type cells. Proliferation, migration and invasion activities were not affected by the expression of TRPM2. TRPM2 seems to be a candidate for gene therapy in glioblastoma cells, since the insertion of TRPM2 into A172 cells can facilitate cell death through Ca2+ increase after H2O2 treatment without increasing malignancy.

MeSH terms

  • Calcium / metabolism
  • Cell Death / drug effects
  • Cell Death / genetics
  • Cell Growth Processes / physiology
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Combined Modality Therapy
  • Genetic Therapy / methods
  • Glioblastoma / genetics*
  • Glioblastoma / metabolism
  • Glioblastoma / pathology
  • Glioblastoma / therapy*
  • Humans
  • Hydrogen Peroxide / pharmacology*
  • Neoplasm Invasiveness
  • Oxidative Stress / genetics
  • TRPM Cation Channels / biosynthesis
  • TRPM Cation Channels / genetics*
  • Transfection

Substances

  • TRPM Cation Channels
  • TRPM2 protein, human
  • Hydrogen Peroxide
  • Calcium