Accepted Articles of Congress

  • Caffeic acid stimulates breast cancer death through Reactive oxygen species (ROS) formation, Caspase activation and mitochondrial membrane potential depletion

  • Ali Karami Robati,1,* Zahra Shahsavari,2 Mohammad Amin Vaezi,3 Banafsheh Safizadeh,4 Farzad Izak Shirian,5 Masoumeh Tavakoli-Yaraki,6
    1. 1) Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
    2. Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
    3. Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
    4. Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
    5. Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
    6. Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.


  • Introduction: This study is aimed to evaluate the potential effect of caffeic acid on the growth of breast cancer cells, beside determining the contributing role of caspases, mitochondria and oxidative status
  • Methods: MCF-7 and MDA-MB-468 breast cancer cells were exposed to varying concentrations of caffeic acid for different periods of time, and the potential cytotoxic effect was measured using the MTT assay. The activity of caspase 3 and caspase 8, as well as the cellular level of reactive oxygen species (ROS) and the level of mitochondrial membrane potential (Δψm), were evaluated in different groups of cells
  • Results: Our findings showed that caffeic acid decreased the percentage of MCF-7 and MDA- MB-468 cells in a manner that depended on the dose and duration of exposure. The death of breast cancer cells induced by caffeic acid was associated with an increase in ROS level in both cell lines. The decrease in mitochondrial membrane potential (Δψm) following caffeic acid treatment suggests that mitochondria dysfunction may be involved in the death of breast cancer cells induced by caffeic acid. Importantly, the activity of caspase 8 increased after treatment, indicating the potential involvement of the extrinsic apoptosis pathway in the inhibition of breast cancer cell growth by caffeic acid
  • Conclusion: Our study highlights the potential pro-apoptotic effect of caffeic acid in both estrogen-positive and estrogen-negative breast cancer cells, which, in conjunction with other evidence, may lead to new insights for more effective therapeutic approaches in breast cancer
  • Keywords: Caffeic acid, Cytotoxicity, Reactive oxygen species, Caspase 3, Caspase 8, Δψm

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