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Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

  • Authors:
    • Kefeng Wu
    • Yi Liu
    • Yingnian Lv
    • Liao Cui
    • Wende Li
    • Jianfa Chen
    • Nian Ci Liang
    • Li Li
  • View Affiliations / Copyright

    Affiliations: Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College, Zhanjiang, Guangdong 524023, P.R. China, Department of General Surgery, 422 Hospital of PLA, Zhanjiang, Guangdong 524009, P.R. China, Institute of Biochemistry and Molecular Biology, Guangdong Medical College, Zhanjiang, Guangdong 524023, P.R. China
    Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 2101-2108
    |
    Published online on: April 3, 2013
       https://doi.org/10.3892/or.2013.2375
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Abstract

Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F), a compound isolated from Pteris semipinnata L. (PsL), inhibits cell proliferation and induces cell apoptosis in several cancer lines. We found that 5F induced apoptosis and G2 phase cell cycle arrest in the CNE-2Z nasopharyngeal carcinoma (NPC) cells, accompanied by a decrease of NF-κB expression. 5F suppressed the viability of CNE-2Z cells in a time- and dose-dependent manner. 5F induced G2/M phase cell cycle arrest, but did not induce p21. Further analysis revealed that CNE-2Z cells harbored two p53 mutations. 5F treatment resulted in mitochondrial apoptosis, associated with increased Bax/Bcl-2 ratio, upregulation of cytochrome c in the cytosol, decreased NF-κB-p65 and increased IκB. Of note, 5F significantly sensitized CNE-2Z cells to cisplatin. 5F did not increase ROS, but reduced ROS production alone or in combination with cisplatin. Our data suggest that 5F is a potential anti-NPC drug for the development of single agent therapy and therapy in combination with cisplatin.
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Copy and paste a formatted citation
Spandidos Publications style
Wu K, Liu Y, Lv Y, Cui L, Li W, Chen J, Liang NC and Li L: Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells. Oncol Rep 29: 2101-2108, 2013.
APA
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J. ... Li, L. (2013). Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells. Oncology Reports, 29, 2101-2108. https://doi.org/10.3892/or.2013.2375
MLA
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J., Liang, N. C., Li, L."Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells". Oncology Reports 29.6 (2013): 2101-2108.
Chicago
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J., Liang, N. C., Li, L."Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells". Oncology Reports 29, no. 6 (2013): 2101-2108. https://doi.org/10.3892/or.2013.2375
Copy and paste a formatted citation
x
Spandidos Publications style
Wu K, Liu Y, Lv Y, Cui L, Li W, Chen J, Liang NC and Li L: Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells. Oncol Rep 29: 2101-2108, 2013.
APA
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J. ... Li, L. (2013). Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells. Oncology Reports, 29, 2101-2108. https://doi.org/10.3892/or.2013.2375
MLA
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J., Liang, N. C., Li, L."Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells". Oncology Reports 29.6 (2013): 2101-2108.
Chicago
Wu, K., Liu, Y., Lv, Y., Cui, L., Li, W., Chen, J., Liang, N. C., Li, L."Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells". Oncology Reports 29, no. 6 (2013): 2101-2108. https://doi.org/10.3892/or.2013.2375
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