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IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation

  • Authors:
    • Kemin Cai
    • Bing Wang
    • Hongmei Dou
    • Ronglan Luan
    • Xueli Bao
    • Jiusheng Chu
  • View Affiliations / Copyright

    Affiliations: Department of Otorhinolaryngology Head and Neck Surgery, Taizhou People's Hospital, Taizhou, Jiangsu 225300, P.R. China, Department of Neurosurgery, Suzhou Kowloon Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Suzhou, Jiangsu 215021, P.R. China
    Copyright: © Cai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4238-4244
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    Published online on: March 31, 2017
       https://doi.org/10.3892/ol.2017.5962
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Abstract

Interleukin (IL)-17A is a T helper (Th)17 cell-secreted cytokine that is able to induce various inflammatory responses. There is emerging evidence that IL-17A is generated in the cancer microenvironment of human nasopharyngeal carcinoma (NPC). However, the role of IL-17A in NPC remains unclear. Thus, the present study aimed to examine the direct influence of IL‑17A stimulation on the proliferation of human NPC cells and identify the underlying molecular mechanisms. Furthermore, E1A binding protein p300 (p300)‑mediated AKT serine/threonine kinase 1 (Akt1) acetylation and its role in regulating the proliferation of NPC cells was investigated. The results of the current study demonstrated that IL‑17A stimulation in vitro increased the proliferation of human NPC cells. Furthermore, Akt1 acetylation was identified to be enhanced in human NPC cells induced by IL‑17A. Additionally, p300 induction was demonstrated to be required for Akt1 acetylation in human NPC cells following exposure to IL‑17A. Functionally, p300‑mediated Akt1 acetylation contributed to the proliferation of human NPC cells stimulated by IL‑17A. In conclusion, the results of the present demonstrate a novel activity of IL‑17A that promotes human NPC cell proliferation via p300‑mediated Akt1 acetylation. This may provide a potential strategy for the treatment of patients with NPC through the inhibition of IL-17A or its receptors.
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Copy and paste a formatted citation
Spandidos Publications style
Cai K, Wang B, Dou H, Luan R, Bao X and Chu J: IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation. Oncol Lett 13: 4238-4244, 2017.
APA
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., & Chu, J. (2017). IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation. Oncology Letters, 13, 4238-4244. https://doi.org/10.3892/ol.2017.5962
MLA
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., Chu, J."IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation". Oncology Letters 13.6 (2017): 4238-4244.
Chicago
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., Chu, J."IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation". Oncology Letters 13, no. 6 (2017): 4238-4244. https://doi.org/10.3892/ol.2017.5962
Copy and paste a formatted citation
x
Spandidos Publications style
Cai K, Wang B, Dou H, Luan R, Bao X and Chu J: IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation. Oncol Lett 13: 4238-4244, 2017.
APA
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., & Chu, J. (2017). IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation. Oncology Letters, 13, 4238-4244. https://doi.org/10.3892/ol.2017.5962
MLA
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., Chu, J."IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation". Oncology Letters 13.6 (2017): 4238-4244.
Chicago
Cai, K., Wang, B., Dou, H., Luan, R., Bao, X., Chu, J."IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation". Oncology Letters 13, no. 6 (2017): 4238-4244. https://doi.org/10.3892/ol.2017.5962
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