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Article

Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways

  • Authors:
    • Meilan Xue
    • Yinlin Ge
    • Chundong Yu
    • Zheng Zheng
    • Xinjia He
    • Jinglan Zhao
  • View Affiliations / Copyright

    Affiliations: Department of Biochemistry and Molecular Biology, Medical College, Qingdao University, Qingdao, Shandong 266021, P.R. China, Department of Laboratory, Women and Children's Hospital of Qingdao, Qingdao, Shandong 266034, P.R. China, Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China, Department of Cardiothoracic Surgery, Qingdao Center Medical Group, Qingdao, Shandong 266033, P.R. China
  • Pages: 978-982
    |
    Published online on: June 1, 2017
       https://doi.org/10.3892/mmr.2017.6678
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Abstract

In the present study, the antitumor effect of n‑3 fatty acid was evaluated, and the effect of docosahexaenoic acid (DHA) on the induction of apoptosis and its underlying mechanism were examined. Flow cytometry and western blot analysis were performed to analyze apoptosis and the expression of protein factors in human breast cancer cells. The data revealed that DHA inhibited the viability of MCF‑7 breast cancer cells in vitro, and promoted cell death by the induction of apoptosis. DHA decreased the expression of B‑cell lymphoma 2 (Bcl‑2), whereas the expression of Bcl‑2‑associated X protein was increased. DHA was also shown to promote the release of Smac/Diablo and cytochrome c from the mitochondria. DHA increased the levels of cleaved caspase‑8, ‑9 and ‑3. Additionally, the protein expression of tumor necrosis factor‑related apoptosis‑inducing ligand, death receptor 4 and Fas were increased following DHA treatment. In conclusion, DHA caused apoptosis of the human breast cancer cells in vitro through the death receptor and mitochondria‑mediated pathways. The results of this study encourage further investigation of the effect of fish oil on the prevention and treatment of human breast cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Xue M, Ge Y, Yu C, Zheng Z, He X and Zhao J: Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways. Mol Med Rep 16: 978-982, 2017.
APA
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., & Zhao, J. (2017). Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways. Molecular Medicine Reports, 16, 978-982. https://doi.org/10.3892/mmr.2017.6678
MLA
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., Zhao, J."Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways". Molecular Medicine Reports 16.1 (2017): 978-982.
Chicago
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., Zhao, J."Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways". Molecular Medicine Reports 16, no. 1 (2017): 978-982. https://doi.org/10.3892/mmr.2017.6678
Copy and paste a formatted citation
x
Spandidos Publications style
Xue M, Ge Y, Yu C, Zheng Z, He X and Zhao J: Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways. Mol Med Rep 16: 978-982, 2017.
APA
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., & Zhao, J. (2017). Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways. Molecular Medicine Reports, 16, 978-982. https://doi.org/10.3892/mmr.2017.6678
MLA
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., Zhao, J."Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways". Molecular Medicine Reports 16.1 (2017): 978-982.
Chicago
Xue, M., Ge, Y., Yu, C., Zheng, Z., He, X., Zhao, J."Apoptosis is induced by docosahexaenoic acid in breast cancer cells via death receptor and mitochondria-mediated pathways". Molecular Medicine Reports 16, no. 1 (2017): 978-982. https://doi.org/10.3892/mmr.2017.6678
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