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

Yong-Ju Liang1, Xu Zhang, Chun-Ling Dai

  • 1State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou 510060, China.

Journal of Biomedicine & Biotechnology
|July 30, 2009
PubMed

Insights

Bullatacin induces apoptosis in multidrug-resistant cells via the mitochondria-dependent pathway. This process involves reactive oxygen species (ROS) and caspase-9 activation, highlighting a potential therapeutic target.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Multidrug resistance (MDR) in cancer cells poses a significant therapeutic challenge.
  • Identifying novel agents that can overcome MDR and induce cancer cell death is crucial.

Purpose of the Study:

  • To investigate the mechanisms of bullatacin-mediated apoptosis in multidrug-resistant cells.
  • To explore the role of reactive oxygen species (ROS) and mitochondrial pathways in bullatacin-induced cell death.

Main Methods:

  • Utilized ABCB1-overexpressing KBv200 cells to study bullatacin effects.
  • Assessed reactive oxygen species (ROS) generation and mitochondrial membrane potential (DeltaPsi(m)).
  • Analyzed caspase activation (caspase-9, caspase-3, caspase-8), PARP cleavage, and cytochrome c release.

Main Results:

  • Bullatacin upregulated ROS and downregulated DeltaPsi(m) in a concentration-dependent manner.
  • Observed cleavage of caspase-9, caspase-3, and PARP, indicating mitochondrial pathway activation.
  • N-acetylcysteine pretreatment reduced ROS and apoptosis; caspase-9 inhibition blocked bullatacin-induced apoptosis.

Conclusions:

  • Bullatacin induces apoptosis in multidrug-resistant cells through the mitochondria-dependent pathway.
  • The mechanism involves ROS generation and subsequent activation of caspase-9.
  • Bullatacin demonstrates potential as an agent to overcome multidrug resistance.

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