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Related Experiment Videos

CD95-mediated apoptosis: no variation in cellular sensitivity during cell cycle progression

A Hueber1, S Durka, M Weller

  • 1Department of Neurology, University of Tübingen, School of Medicine, Germany.

FEBS Letters
|August 28, 1998
PubMed
Summary

Cell cycle phase does not affect CD95-mediated apoptosis sensitivity in glioma, Jurkat, HeLa, or HepG2 cells. This finding suggests cell cycle status is not a reliable predictor for CD95-ligand-induced cell death.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Previous studies suggested CD95-mediated apoptosis sensitivity varies with cell cycle progression.
  • CD95, also known as Fas receptor, plays a critical role in programmed cell death.

Purpose of the Study:

  • To investigate whether cell cycle phase influences CD95 expression and susceptibility to CD95 ligand-induced apoptosis in human glioma and other cancer cell lines.
  • To determine if cell cycle progression is a predictor of vulnerability to CD95-mediated apoptosis.

Main Methods:

  • Utilized three human glioma cell lines with varying p53 status.
  • Induction of growth arrest and synchronous cell cycle re-entry via prolonged serum deprivation.
  • Assessed cell surface CD95 expression and susceptibility to CD95 ligand-induced apoptosis across different cell cycle phases.

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  • Compared findings with Jurkat T cells, HeLa cervical carcinoma, and HepG2 hepatocellular carcinoma cells.

    • Main Results:

    • Glioma cell lines, regardless of p53 status, did not show cell cycle-related changes in CD95 expression or apoptosis susceptibility.
    • CD95 expression and apoptosis sensitivity remained constant during cell cycle progression in Jurkat, HeLa, and HepG2 cells.
    • In contrast, cell cycle-specific activity was observed for conventional cancer chemotherapy drugs.

    Conclusions:

    • Cell cycle phase is not a significant predictor of sensitivity to CD95 ligand-induced apoptosis in the studied cancer cell lines.
    • The findings do not support a role for cell cycle regulation in modulating vulnerability to CD95-mediated apoptosis.