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Article

Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells

  • Authors:
    • Xiaoqi Sun
    • Hong Zhang
    • Yingyu Zhang
    • Qi Yang
    • Shujie Zhao
  • View Affiliations / Copyright

    Affiliations: Faculty of Clinical Medicine, Changchun Medical College, Changchun, Jilin 130031, P.R. China, Department of Imaging, The First Hospital of Jilin University, Jilin University, Changchun, Jilin 130021, P.R. China, Department of Endocrinology, The Second Hospital of Jilin University, Jilin University, Changchun, Jilin 13000, P.R. China
  • Pages: 2278-2286
    |
    Published online on: July 26, 2018
       https://doi.org/10.3892/or.2018.6602
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Abstract

Astilbin exhibits several pharmacological activities, including hypoglycemic, anti-oxidant and anti-inflammatory properties. The aim of the present study was to investigate the pro-apoptotic activities of astilbin on breast cancer in cells and mice. It was demonstrated that astilbin significantly reduced the cell viability, increased the cell apoptosis rate, suppressed the migration ability, caused the dissipation of the mitochondrial membrane potential and induced the overaccumulation of intracellular reactive oxygen species in MCF-7 and MDA-MB-231 cells after 12 or 24 h of exposure. Data obtained from western blotting suggested that astilbin suppressed the expression levels of B-cell lymphoma 2 (Bcl-2), while it increased the expression levels of cleaved caspase-3, -8 and -9, and Bcl-2-associated X protein in breast carcinoma cells. Furthermore, astilbin inhibited the growth of MCF-7-xenografted tumors in nude mice without influencing their bodyweights or organ (liver, spleen and kidney) functions. Additionally, astilbin enhanced the expression of pro-apoptotic proteins and suppressed the expression of anti-apoptotic proteins in tumor tissues. All these results revealed that astilbin exhibits pro-apoptotic properties in breast carcinoma cells via modulation of the caspase-dependent pathway, which highlights the feasibility of astilbin as a candidate agent for breast cancer treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Sun X, Zhang H, Zhang Y, Yang Q and Zhao S: Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells. Oncol Rep 40: 2278-2286, 2018.
APA
Sun, X., Zhang, H., Zhang, Y., Yang, Q., & Zhao, S. (2018). Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells. Oncology Reports, 40, 2278-2286. https://doi.org/10.3892/or.2018.6602
MLA
Sun, X., Zhang, H., Zhang, Y., Yang, Q., Zhao, S."Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells". Oncology Reports 40.4 (2018): 2278-2286.
Chicago
Sun, X., Zhang, H., Zhang, Y., Yang, Q., Zhao, S."Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells". Oncology Reports 40, no. 4 (2018): 2278-2286. https://doi.org/10.3892/or.2018.6602
Copy and paste a formatted citation
x
Spandidos Publications style
Sun X, Zhang H, Zhang Y, Yang Q and Zhao S: Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells. Oncol Rep 40: 2278-2286, 2018.
APA
Sun, X., Zhang, H., Zhang, Y., Yang, Q., & Zhao, S. (2018). Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells. Oncology Reports, 40, 2278-2286. https://doi.org/10.3892/or.2018.6602
MLA
Sun, X., Zhang, H., Zhang, Y., Yang, Q., Zhao, S."Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells". Oncology Reports 40.4 (2018): 2278-2286.
Chicago
Sun, X., Zhang, H., Zhang, Y., Yang, Q., Zhao, S."Caspase-dependent mitochondrial apoptotic pathway is involved in astilbin-mediated cytotoxicity in breast carcinoma cells". Oncology Reports 40, no. 4 (2018): 2278-2286. https://doi.org/10.3892/or.2018.6602
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