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Signalling steps in apoptosis by ether lipids.

L A Smets1, H Van Rooij, G S Salomons

  • 1Division of Experimental Therapy, The Netherlands Cancer Institute/Antoni van Leeuwenhoekhuis, Amsterdam, The Netherlands. LOU@nki.edu

Apoptosis : an International Journal on Programmed Cell Death
|November 25, 2003
PubMed
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Antineoplastic ether lipids induce apoptosis via reactive oxygen species, independent of p53. Glutathione-dependent antioxidant defense determines sensitivity to ether lipids, stress, and radiation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Cancer Research

Background:

  • Apoptosis, or programmed cell death, is crucial for development and disease.
  • Ether lipids are a class of antineoplastic agents with potential therapeutic applications.
  • Understanding the mechanisms of apoptosis induction is key to developing effective cancer therapies.

Purpose of the Study:

  • To investigate the mechanisms of apoptosis induction by the ether lipid ET-18-OCH3 (ALP).
  • To compare apoptosis sensitivity in p53 wild-type and mutated cells.
  • To identify factors contributing to ether lipid resistance.

Main Methods:

  • Utilized sensitive S49wt and resistant S49ar mouse lymphoma cells, and L1210 cells.
  • Assessed apoptosis induction by ALP and various stress factors.

Related Experiment Videos

  • Measured [3H]-ALP uptake, membrane properties, and glutathione peroxidase (GSH-Px) activity.
  • Used L-buthionine-S-R-sulfoximine (L-BSO) to deplete glutathione.

    • Main Results:

    • Ether lipid-resistant cells showed cross-resistance to extracellular stress and radiation but not physiological apoptotic signals.
    • Reduced ALP uptake was observed in resistant cells, independent of membrane composition.
    • Increased GSH-Px activity in resistant cells was linked to resistance, which was reversed by glutathione depletion.
    • Apoptosis induction by ether lipids was independent of p53 status.

    Conclusions:

    • Ether lipids induce apoptosis through a unique physico-chemical stress mediated by reactive oxygen species.
    • Glutathione-dependent antioxidant defense is a critical determinant of sensitivity to ether lipids, extracellular stress, and ionizing radiation.
    • These findings offer insights into ether lipid resistance mechanisms and potential therapeutic strategies.