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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics
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Article

Pristimerin induces caspase-dependent apoptosis in MDA-MB-231 cells via direct effects on mitochondria

Chin-Chung Wu, Mei-Ling Chan, Wen-Ying Chen, Ching-Yi Tsai, Fang-Rong Chang and Yang-Chang Wu
Chin-Chung Wu
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Mei-Ling Chan
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Wen-Ying Chen
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Ching-Yi Tsai
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Fang-Rong Chang
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Yang-Chang Wu
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DOI: 10.1158/1535-7163.MCT-05-0027 Published August 2005
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Abstract

Pristimerin, a naturally occurring triterpenoid, has been shown to cause cytotoxicity in several cancer cell lines. However, the mechanism for the cytotoxic effect of pristimerin was never explored. In the present study, human breast cancer MDA-MB-231 cells treated with pristimerin (1 and 3 μmol/L) showed rapid induction of apoptosis, as indicated by caspase activation, DNA fragmentation, and morphologic changes. Pretreatment of a pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk) completely prevented pristimerin-induced apoptosis. Treatment of tumor cells with pristimerin resulted in a rapid release of cytochrome c from mitochondria, which preceded caspase activation and the decrease of mitochondrial membrane potential. In addition, neither benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone nor permeability transition pore inhibitor cyclosporin A markedly prevented pristimerin-induced mitochondrial cytochrome c release. Pristimerin did not significantly alter the protein level of Bcl-2 family members (Bcl-2, Bcl-XL, and Bax), nor did it induce Bax translocation. Moreover, Bcl-2 overexpression fails to prevent pristimerin-induced apoptosis. The generation of reactive oxygen species in MDA-MB-231 cells was also not affected by pristimerin. In a cell-free system, pristimerin induced cytochrome c release from isolated mitochondria. Taken together, these results suggested that pristimerin is a novel mitochondria-targeted compound and may be further evaluated as a chemotherapeutic agent for human cancer.

Keywords:
  • pristimerin
  • cancer
  • mitochondria
  • cytochrome c

Footnotes

  • Grant support: National Science Council of Taiwan (NSC 92-2320-B-037-026).

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted June 14, 2005.
    • Received January 21, 2005.
    • Revision received May 27, 2005.
  • American Association for Cancer Research
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Molecular Cancer Therapeutics: 4 (8)
August 2005
Volume 4, Issue 8
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Pristimerin induces caspase-dependent apoptosis in MDA-MB-231 cells via direct effects on mitochondria
Chin-Chung Wu, Mei-Ling Chan, Wen-Ying Chen, Ching-Yi Tsai, Fang-Rong Chang and Yang-Chang Wu
Mol Cancer Ther August 1 2005 (4) (8) 1277-1285; DOI: 10.1158/1535-7163.MCT-05-0027

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Pristimerin induces caspase-dependent apoptosis in MDA-MB-231 cells via direct effects on mitochondria
Chin-Chung Wu, Mei-Ling Chan, Wen-Ying Chen, Ching-Yi Tsai, Fang-Rong Chang and Yang-Chang Wu
Mol Cancer Ther August 1 2005 (4) (8) 1277-1285; DOI: 10.1158/1535-7163.MCT-05-0027
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Molecular Cancer Therapeutics
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