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Cytoskeletal disruption is the key factor that triggers apoptosis in okadaic acid-treated neuroblastoma cells

A G Cabado1, F Leira, M R Vieytes

  • 1ANFACO-CECOPESCA, Campus Universitario de Vigo, 36310, Vigo (Pontevedra), Spain. agcabado@ANFACO.es

Archives of Toxicology
|December 4, 2003
PubMed

Insights

Okadaic acid (OA) triggers apoptosis by disrupting the cytoskeleton and mitochondrial function in BE(2)-M17 cells. While cytoskeletal changes are key, mitochondrial potential collapse is accessory to OA-induced cell death.

Area of Science:

  • Cell Biology
  • Biochemistry

Background:

  • Okadaic acid (OA) is recognized as a tumor promoter.
  • OA has been shown to induce apoptosis in various cell models.

Purpose of the Study:

  • To investigate the specific molecular pathways involved in OA-induced apoptosis in BE(2)-M17 cells.
  • To differentiate between essential and accessory roles of cellular events in OA-triggered cell death.

Main Methods:

  • Utilized a combination of pharmacological agents and apoptosis-related assays.
  • Monitored F-actin cytoskeleton integrity, caspase-3 activation, mitochondrial membrane potential, DNA fragmentation, and Bcl-2/Bax protein levels.

Main Results:

  • OA induced apoptosis through F-actin disruption, caspase-3 activation, mitochondrial potential collapse, DNA fragmentation, and altered Bcl-2/Bax levels.
  • Cytoskeletal changes, caspase-3 activation, and DNA fragmentation were irreversible by tested agents.
  • Mitochondrial potential and Bcl-2/Bax level changes were preventable, indicating their accessory role.

Conclusions:

  • Mitochondrial membrane potential collapse is accessory to OA-induced apoptosis execution.
  • Apoptosis execution is directly dependent on cytoskeletal changes.
  • Mitochondrial changes are linked to Bcl-2 protein interactions, with cytochrome c release as a late event.

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