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Involvement of p53 in cell death following cell cycle arrest and mitotic catastrophe induced by rotenone

António Pedro Gonçalves1, Valdemar Máximo, Jorge Lima

  • 1IBMC-Instituto de Biologia Molecular e Celular, Universidade do Porto, Rua do Campo Alegre 823, 4150-180 Porto, Portugal. apgoncalves@ibmc.up.pt

Biochimica Et Biophysica Acta
|January 13, 2011
PubMed

Insights

Rotenone, a mitochondrial inhibitor, induces cancer cell death and cell cycle arrest. While p53 is crucial for rotenone-induced cell death, its effects are independent of reactive oxygen species production.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Rotenone is a natural plant extract widely recognized as a mitochondrial complex I inhibitor.
  • Its potential anti-cancer properties warrant investigation into its mechanisms of action in cancer cells.

Purpose of the Study:

  • To investigate the cell death-inducing effects of rotenone in cancer cell lines.
  • To elucidate the role of the tumor suppressor p53 in rotenone-induced cell death.
  • To determine if rotenone's effects are dependent on reactive oxygen species production.

Main Methods:

  • Treatment of various cancer cell lines with rotenone and staurosporine.
  • Analysis of cell death, cell cycle arrest, mitotic catastrophe, and senescence.
  • Assessment of p53 protein expression, phosphorylation, and nuclear localization.
  • Evaluation of rotenone's effects on mitochondrial DNA-depleted cells.

Main Results:

  • Rotenone inhibits cancer cell growth by inducing cell death, cell cycle arrest, and mitotic catastrophe.
  • Staurosporine synergistically enhances rotenone's growth inhibitory effects.
  • Functional p53 is essential for extensive cell death following rotenone-induced mitotic catastrophe.
  • Rotenone induces cell death and cell cycle arrest in both mtDNA-depleted and wild-type cells, independent of reactive oxygen species generation.

Conclusions:

  • Rotenone exhibits multiple anti-cancer effects, acting as an anti-mitotic drug.
  • The tumor suppressor p53 plays a critical role in mediating rotenone-induced extensive cell death.
  • Rotenone's cytotoxic effects on cancer cells are not dependent on reactive oxygen species production.

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