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Blocking mitochondrial permeability transition prevents p53 mitochondrial translocation during skin tumor promotion

Jianfeng Liu1, Daret K St Clair, Xin Gu

  • 1Department of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA 71130, USA.

FEBS Letters
|March 25, 2008
PubMed

Insights

Blocking mitochondrial permeability transition prevents tumor suppressor p53 from entering mitochondria, thereby suppressing apoptosis. This finding highlights the role of mitochondrial permeability in p53-mediated cell death pathways.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The tumor suppressor p53 plays a crucial role in apoptosis.
  • p53 can translocate into mitochondria to initiate apoptosis.

Purpose of the Study:

  • To investigate the effect of blocking mitochondrial permeability transition pore on p53 mitochondrial translocation and apoptosis.
  • To determine if mitochondrial permeability transition is essential for p53 mitochondrial translocation.

Main Methods:

  • Utilized skin epidermal JB6 cells and skin tissues.
  • Employed cyclosporine A (CsA) and bongkrekic acid (BA) to block the mitochondrial permeability transition pore.
  • Assessed TPA-induced p53 translocation, mitochondrial membrane potential, and Complex I activity.

Main Results:

  • CsA and BA effectively blocked TPA-induced p53 translocation into mitochondria.
  • Inhibition of p53 translocation protected against loss of mitochondrial membrane potential and Complex I activity.
  • Blocking mitochondrial permeability transition ultimately suppressed apoptosis.

Conclusions:

  • Mitochondrial permeability transition is a required step for p53 mitochondrial translocation.
  • Targeting mitochondrial permeability transition may offer a strategy to modulate p53-mediated apoptosis.

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