FEBS Letters
Volume 582, Issue 9 , Pages 1319-1324, 16 April 2008

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

Edited by Varda Rotter

  • Jianfeng Liu

      Affiliations

    • Department of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA 71130, United States
    • ,
  • Daret K. St. Clair

      Affiliations

    • Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, United States
    • ,
  • Xin Gu

      Affiliations

    • Department of Pathology, LSU Health Sciences Center, Shreveport, LA 71130, United States
    • ,
  • Yunfeng Zhao

      Affiliations

    • Department of Pharmacology, Toxicology and Neuroscience, LSU Health Sciences Center, Shreveport, LA 71130, United States
    • Corresponding Author InformationCorresponding author. Fax: +1 318 675 7857.

Received 25 January 2008; received in revised form 9 March 2008; accepted 11 March 2008. published online 20 March 2008.

Abstract 

The tumor suppressor p53 can translocate into mitochondria and activate apoptosis. Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues. Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis. Thus, our results suggest that mitochondrial permeability transition is required for p53 mitochondrial translocation.

Keywords: p53, Mitochondria, Apoptosis

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PII: S0014-5793(08)00242-1

doi:10.1016/j.febslet.2008.03.013

FEBS Letters
Volume 582, Issue 9 , Pages 1319-1324, 16 April 2008

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