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The cytoskeleton as a subcellular target of the antineoplastic drug lonidamine

W Malorni1, S Meschini, P Matarrese

  • 1Department of Ultrastructures, Istituto Superiore di Sanità, Rome, Italy.

Anticancer Research
|November 1, 1992
PubMed

Insights

Lonidamine (LND) disrupts cell structure by altering the cytoskeleton, affecting actin, microtubules, and intermediate filaments. These changes correlate with cell surface damage and reduced cell viability, indicating LND

Area of Science:

  • Cell Biology
  • Biochemistry
  • Cancer Research

Background:

  • Lonidamine (LND) is a potent antiproliferative agent impacting cellular energy metabolism.
  • LND's mechanism of action, particularly its effect on cell surface and cytoskeleton, requires further elucidation.

Purpose of the Study:

  • To investigate the effects of Lonidamine (LND) on the cell surface and major cytoskeletal components.
  • To determine if cytoskeletal alterations contribute to LND's cytotoxic effects.

Main Methods:

  • Immunocytochemical and ultrastructural analysis were employed.
  • Two distinct cell lines, A431 (epithelial squamous carcinoma) and M14 (melanoma), were utilized.
  • Cells were treated with 0.8 mM LND for 8 hours.

Main Results:

  • LND treatment caused significant F-actin rearrangement and stress fiber disappearance.
  • Microtubules reorganized into perinuclear patches of tubulin.
  • Intermediate filament alterations varied between cell lines.
  • Observed cytoskeletal changes were early events linked to cell surface alterations and decreased cell viability.

Conclusions:

  • Cytoskeletal elements, including actin microfilaments, microtubules, and intermediate filaments, are targets of Lonidamine (LND).
  • LND-induced cytoskeletal disruption contributes to its antiproliferative and cytotoxic effects.
  • These findings suggest a multifaceted mechanism of action for LND involving cellular structural integrity.

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