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Article

Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway

  • Authors:
    • Ben‑Shan Li
    • Ji‑Yi Huang
    • Jing Guan
    • Long‑Hua Chen
  • View Affiliations / Copyright

    Affiliations: Department of Radiation Oncology, Nanfang Hospital Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of E.N.T., People's Hospital of Jiangmen, Jiangmen, Guangdong 529000, P.R. China, Department of Oncology, People's Hospital of Jiangmen, Jiangmen, Guangdong 529000, P.R. China
  • Pages: 552-558
    |
    Published online on: May 10, 2018
       https://doi.org/10.3892/ol.2018.8688
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Abstract

Nasopharyngeal carcinoma (NPC) is a type of cancer that is characterized by increased invasiveness, metastatic potential and tumor recurrence. Camptothecin has been demonstrated to exhibit anticancer activity. However, the potential underlying molecular mechanisms mediated by camptothecin in NPC cells remain elusive. In the present study, the efficacy of camptothecin for NPC was investigated in vitro and in vivo. Additionally, the potential signaling pathway mediated by camptothecin in NPC cells was also examined. The results indicated that the viability and aggressiveness of NPC cells were suppressed by camptothecin treatment in a dose‑dependent manner. Camptothecin administration downregulated the expression levels of cell‑cycle‑associated proteins including cyclin 1, cyclin‑dependent kinase (CDK)1 and CDK2 in NPC cells. Expression levels of migration‑associated proteins including vimentin, fibronectin and epithelial cadherin were regulated by camptothecin treatment in NPC cells. Additionally, camptothecin inhibited the expression of transforming growth factor‑β (TGF‑β), phosphoinositide 3‑kinase (PI3K) and protein kinase B (AKT), whereas TGF‑β overexpression abrogated camptothecin‑mediated inhibition of PI3K and AKT expression and camptothecin‑mediated inhibition of the viability and aggressiveness of NPC cells. Camptothecin significantly inhibited tumor growth and increased survival times in a mouse model of cancer. In conclusion, these results indicate that camptothecin treatment may inhibit the viability of NPC cells and aggressiveness by regulating the TGF‑β‑induced PI3K/AKT signaling pathways, which in turn may be a potential molecular target for the treatment of NPC.
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Copy and paste a formatted citation
Spandidos Publications style
Li BS, Huang JY, Guan J and Chen LH: Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway. Oncol Lett 16: 552-558, 2018.
APA
Li, B., Huang, J., Guan, J., & Chen, L. (2018). Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway. Oncology Letters, 16, 552-558. https://doi.org/10.3892/ol.2018.8688
MLA
Li, B., Huang, J., Guan, J., Chen, L."Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway". Oncology Letters 16.1 (2018): 552-558.
Chicago
Li, B., Huang, J., Guan, J., Chen, L."Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway". Oncology Letters 16, no. 1 (2018): 552-558. https://doi.org/10.3892/ol.2018.8688
Copy and paste a formatted citation
x
Spandidos Publications style
Li BS, Huang JY, Guan J and Chen LH: Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway. Oncol Lett 16: 552-558, 2018.
APA
Li, B., Huang, J., Guan, J., & Chen, L. (2018). Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway. Oncology Letters, 16, 552-558. https://doi.org/10.3892/ol.2018.8688
MLA
Li, B., Huang, J., Guan, J., Chen, L."Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway". Oncology Letters 16.1 (2018): 552-558.
Chicago
Li, B., Huang, J., Guan, J., Chen, L."Camptothecin inhibits the progression of NPC by regulating TGF‑β‑induced activation of the PI3K/AKT signaling pathway". Oncology Letters 16, no. 1 (2018): 552-558. https://doi.org/10.3892/ol.2018.8688
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