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Bullatacin triggered ABCB1-overexpressing cell apoptosis via the mitochondrial-dependent pathway.

This paper was to explore bullatacin-mediated multidrug-resistant cell apoptosis at extremely low concentration. To investigate its precise mechanisms, the pathway of cell apoptosis induced by bullatacin was examined. Bullatacin causes an upregulation of ROS and a downregulation of DeltaPsi(m) in a...

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Published in:Journal of Biomedicine & Biotechnology pp. 9p - 10
Main Authors: Liang Y, Zhang X, Dai C, Zhang J, Yan Y, Zeng M, Chen L, Fu L
Format: diagnostic images research tables/charts Journal Article
Published: Wiley-Blackwell 2009 Regular Issue
Online Access:View this record in EBSCOhost
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        11107243
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      jtl: Journal of Biomedicine & Biotechnology
      issn: 11107243
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      dt: 2009 Regular Issue
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        atl: Bullatacin triggered ABCB1-overexpressing cell apoptosis via the mitochondrial-dependent pathway.
      aug:
        au:
          Liang Y
          Zhang X
          Dai C
          Zhang J
          Yan Y
          Zeng M
          Chen L
          Fu L
        affil: State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou 510060, China.
      sug:
        subj:
          Antineoplastic Agents
          Apoptosis
          Gene Expression
          Genes
          Mitochondria
          Proteins
          Acetylcysteine
          Cells
          Funding Source
          Staining and Labeling
          T-Tests
          Tissue Culture Techniques
          Human
      ab: This paper was to explore bullatacin-mediated multidrug-resistant cell apoptosis at extremely low concentration. To investigate its precise mechanisms, the pathway of cell apoptosis induced by bullatacin was examined. Bullatacin causes an upregulation of ROS and a downregulation of DeltaPsi(m) in a concentration-dependent manner in ABCB1-overexpressing KBv200 cells. In addition, cleavers of caspase-9, caspase-3, and PARP were observed following the release of cytochrome c from mitochondria after bullatacin treatment. However, neither cleavage of caspase-8 nor change of expression level of bcl-2, bax and Fas was observed by the same treatment. Pretreating KBv200 cells with N-acetylcysteine, an antioxidant modulator, resulted in a significant reduction of ROS generation and cell apoptosis induced by bullatacin. Bullatacin-induced apoptosis was antagonized by z-LEHD-fmk, a caspase-9 inhibitor, but not by z-IETD-fmk, a caspase-8 inhibitor. These implied that apoptosis of KBv200 cells induced by bullatacin was associated with the mitochondria-dependent pathway that was limited to activation of apical caspase-9.
      pubtype: Academic Journal
      doctype:
        diagnostic images
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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