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Enhanced apoptosis through farnesol inhibition of phospholipase D signal transduction

Marcia M Taylor1, Kendra Macdonald, Andrew J Morris

  • 1Atlantic Research Centre, Dalhousie University, Halifax, Canada.

The FEBS Journal
|September 24, 2005
PubMed

Insights

Farnesol induces apoptosis in cancer cells, but this effect is blocked by lipids like phosphatidylcholine and diacylglycerol. Inhibiting lipid breakdown enhances farnesol

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cancer Research

Background:

  • Farnesol, a cholesterol metabolite, induces apoptosis in tumorigenic cells.
  • Lipids such as phosphatidylcholine (PC), phosphatidic acid (PA), and diacylglycerol (DAG) can counteract farnesol-induced apoptosis.

Purpose of the Study:

  • To investigate the role of lipid metabolism in farnesol-mediated apoptosis.
  • To elucidate the mechanism by which farnesol induces cell death in cancer.

Main Methods:

  • Investigated the effects of various lipids on farnesol-induced apoptosis.
  • Utilized primary alcohols to inhibit PC catabolism by phospholipase D.
  • Employed plasmid transformation with PA phosphatase LPP3 and its mutant.
  • Performed in vitro enzyme activity assays.

Main Results:

  • PC, PA, and DAG protected against farnesol-induced apoptosis.
  • Inhibition of PC catabolism by primary alcohols augmented farnesol-induced apoptosis.
  • Exogenous PC did not prevent this augmentation, but DAG was protective.
  • Transformation with active LPP3 prevented farnesol-mediated apoptosis, but not with an inactive mutant.
  • Farnesol did not directly inhibit LPP3 PA phosphatase activity in vitro.

Conclusions:

  • Farnesol's apoptotic effect is modulated by lipid metabolism.
  • Farnesol likely inhibits a diacylglycerol (DAG) pool generated by phospholipase D signaling.
  • This inhibition targets an antiapoptotic/pro-proliferative pathway, suggesting a novel mechanism for farnesol in cancer therapy.

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