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Fas (APO-1/CD95) signaling pathway is intact in radioresistant human glioma cells

G L Yount1, K S Levine, H Kuriyama

  • 1Preuss Laboratory for Molecular Neuro-oncology, Brain Tumor Research Center, Department of Neurological Surgery, University of California San Francisco, 94143, USA.

Cancer Research
|March 30, 1999
PubMed

Insights

Glioblastoma cells resist radiation but can undergo programmed cell death (apoptosis) via the Fas pathway. Ceramide or anti-Fas antibody treatment effectively induces this Fas-mediated apoptosis, independent of p53.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Death Research

Background:

  • Glioblastoma multiforme is a primary brain tumor known for its resistance to radiation therapy.
  • Radiation-induced apoptosis can be triggered by DNA damage or ceramide-mediated Fas signaling.
  • U-87 MG, SF126, and T98G are glioblastoma cell lines exhibiting characteristic radioresistance.

Purpose of the Study:

  • To investigate the susceptibility of radioresistant glioblastoma cells to Fas-mediated apoptosis.
  • To determine if ceramide or anti-Fas antibody can induce cell death in these resistant cell lines.
  • To explore the role of the p53 pathway in Fas-mediated cell death in glioma cells.

Main Methods:

  • Treatment of glioblastoma cell lines (U-87 MG, SF126, T98G) with anti-Fas antibody.
  • Treatment of glioblastoma cell lines with exogenous ceramide.
  • Assessment of Fas-mediated cell death and p53-independence.

Main Results:

  • The radioresistant glioblastoma cell lines were susceptible to Fas-mediated cell death.
  • Treatment with anti-Fas antibody or exogenous ceramide effectively induced apoptosis.
  • Fas-mediated cell death in these glioma cells was found to be p53-independent.

Conclusions:

  • Apoptosis can be induced by ceramide and mediated through the Fas pathway in glioma cells.
  • High-dose ionizing radiation does not effectively trigger the Fas pathway in these radioresistant cells.
  • Targeting the Fas pathway presents a potential therapeutic strategy for glioblastoma.

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