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Essential roles of caspases and their upstream regulators in rotenone-induced apoptosis

Jihjong Lee1, Ming-Shyan Huang, I-Chi Yang

  • 1Graduate Institute of Veterinary Medicine, College of Biological Resources and Agriculture, National Taiwan University, Taipei, Taiwan.

Biochemical and Biophysical Research Communications
|April 12, 2008
PubMed

Insights

Rotenone triggers oral cancer cell death by activating caspases (cell death proteases) and the p53-Bax pathway, leading to apoptosis. Antioxidants can block this rotenone-induced cell death.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Toxicology

Background:

  • Cytotoxicity is a critical factor in cancer progression and treatment.
  • Understanding the molecular mechanisms of cell death induced by toxins like rotenone is essential for therapeutic development.

Purpose of the Study:

  • To investigate the role of caspases and their upstream regulators in rotenone-induced cytotoxicity in oral cancer cells.
  • To elucidate the specific apoptotic pathways activated by rotenone exposure.

Main Methods:

  • Oral cancer cell lines and normal oral mucosal fibroblasts were treated with varying doses of rotenone.
  • Flow cytometry was used to analyze DNA content and cell cycle arrest.
  • Western blotting was employed to detect the activation of caspase pathways and key proteins like p53 and Bax.
  • The effect of antioxidants on rotenone-induced apoptosis was assessed.

Main Results:

  • Rotenone inhibited oral cancer cell proliferation in a dose-dependent manner.
  • Rotenone induced apoptosis and G2/M cell cycle arrest.
  • Both caspase-8 and caspase-9 pathways were activated, along with p53 and Bax induction.
  • Antioxidants such as glutathione, N-acetylcysteine, and tiron inhibited rotenone-induced apoptosis.

Conclusions:

  • Caspases and their upstream regulators are significantly involved in rotenone-induced cytotoxicity in oral cancer cells.
  • Rotenone triggers apoptosis through both caspase-8 and caspase-9 dependent pathways.
  • The p53-Bax pathway plays a role in rotenone-mediated apoptosis, which can be modulated by antioxidants.

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