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Article

Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway

  • Authors:
    • Min‑Lun Nan
    • Xue Wang
    • Hai‑Jun Li
    • De‑Hai Yu
    • Wen‑Yi Sun
    • Hong‑Mei Xu
    • Yu‑Fang He
    • Quan‑Cheng Zhao
  • View Affiliations / Copyright

    Affiliations: Institute of Phytochemistry, Jilin Academy of Chinese Medicine Sciences, Changchun, Jilin 130000, P.R. China, College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, Jilin 130042, P.R. China, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, Cancer Center, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, Department of Clinical Pharmacy and Pharmaceutical Management, School of Pharmaceutical Sciences in Jilin University, Changchun, Jilin 130021, P.R. China, Department of Obstetrics, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
  • Pages: 630-637
    |
    Published online on: October 24, 2018
       https://doi.org/10.3892/ol.2018.9616
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Abstract

In the present study, the functions and mechanisms of rotundic acid (RA) underlying its induction of apoptosis in caspase‑3‑transfected MCF‑7 human breast cancer cells (Cas3‑MCF‑7 cells) were investigated. RA induced apoptosis in Cas3‑MCF‑7 cells more efficiently compared with that in MCF‑7 cells transfected with control plasmid. The results from an MTT assay demonstrated that RA effectively inhibited Cas3‑MCF‑7 cell viability in a dose‑dependent manner and induced cell apoptosis via caspase‑3 activity within 12 to 48 h. Western blotting and fluorescence‑activated cell sorting demonstrated that RA initiated Cas3‑MCF‑7 cell apoptosis via p53 activation. The silencing of the p53 gene in the Cas3‑MCF‑7 cell line led to decreased RA‑induced Cas3‑MCF‑7 cell caspase‑3 activity and cell apoptosis. Collectively, the results of the present study indicate that caspase‑3 serves a critical function in rotundic acid‑induced apoptosis, and suggest that caspase‑3 deficiency may contribute to the chemotherapy‑resistance of breast cancer. Reconstitution of caspase‑3 sensitizes MCF‑7 breast cancer cells to chemotherapy. RA has the potential for development as a novel drug combined with reconstitution of caspase‑3 gene therapy for the treatment of human breast cancer with caspase‑3 deficiency.
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Copy and paste a formatted citation
Spandidos Publications style
Nan ML, Wang X, Li HJ, Yu DH, Sun WY, Xu HM, He YF and Zhao QC: Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway. Oncol Lett 17: 630-637, 2019.
APA
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H. ... Zhao, Q. (2019). Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway. Oncology Letters, 17, 630-637. https://doi.org/10.3892/ol.2018.9616
MLA
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H., He, Y., Zhao, Q."Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway". Oncology Letters 17.1 (2019): 630-637.
Chicago
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H., He, Y., Zhao, Q."Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway". Oncology Letters 17, no. 1 (2019): 630-637. https://doi.org/10.3892/ol.2018.9616
Copy and paste a formatted citation
x
Spandidos Publications style
Nan ML, Wang X, Li HJ, Yu DH, Sun WY, Xu HM, He YF and Zhao QC: Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway. Oncol Lett 17: 630-637, 2019.
APA
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H. ... Zhao, Q. (2019). Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway. Oncology Letters, 17, 630-637. https://doi.org/10.3892/ol.2018.9616
MLA
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H., He, Y., Zhao, Q."Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway". Oncology Letters 17.1 (2019): 630-637.
Chicago
Nan, M., Wang, X., Li, H., Yu, D., Sun, W., Xu, H., He, Y., Zhao, Q."Rotundic acid induces Cas3‑MCF‑7 cell apoptosis through the p53 pathway". Oncology Letters 17, no. 1 (2019): 630-637. https://doi.org/10.3892/ol.2018.9616
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