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Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma

  • Authors:
    • Yunhe Ju
    • Chuanzheng Sun
    • Xiaoli Wang
  • View Affiliations / Copyright

    Affiliations: Department of Radiotherapy, The Third Affiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan Province, Kunming, Yunnan 650000, P.R. China, Department of Head and Neck Surgery, The Third Affiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan Province, Kunming, Yunnan 650000, P.R. China
    Copyright: © Ju et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 613-620
    |
    Published online on: November 23, 2018
       https://doi.org/10.3892/etm.2018.7007
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Abstract

Nasopharyngeal carcinoma (NPC) is a common malignant disease that is prevalent in Asian countries. Atypical chemokine receptor 4 (ACKR4) binds to various chemokines, including C‑C motif chemokine ligand (CCL)19, CCL21, CCL25 and C‑X‑C motif chemokine ligand 13, without inducing downstream signaling transduction. However, the role of ACKR4 in modulating NPC development remains unclear. In the present study, the effects of ACKR4 on NPC growth, invasion and metastasis were investigated, as well as the endogenous mechanisms through which ACKR4 mediates NPC development. The results demonstrated that ACKR4 was downregulated in human NPC tumor tissues, as compared with that in adjacent normal tissue. In a subcutaneous tumor animal model, the knockdown of ACKR4 enhanced NPC invasion and metastasis. Furthermore, CCL21 was accumulated in ACKR4 knockdown tumors. In vitro, the loss of ACKR4 increased CCL21‑mediated SUNE‑1 cell proliferation, epithelial‑mesenchymal transition and invasion. In conclusion, the loss of ACKR4 promoted CCL21‑mediated NPC development; thus, neutralizing CCL21 in NPC with low ACKR4 expression may be a novel treatment strategy.
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Copy and paste a formatted citation
Spandidos Publications style
Ju Y, Sun C and Wang X: Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma. Exp Ther Med 17: 613-620, 2019.
APA
Ju, Y., Sun, C., & Wang, X. (2019). Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma. Experimental and Therapeutic Medicine, 17, 613-620. https://doi.org/10.3892/etm.2018.7007
MLA
Ju, Y., Sun, C., Wang, X."Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma". Experimental and Therapeutic Medicine 17.1 (2019): 613-620.
Chicago
Ju, Y., Sun, C., Wang, X."Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma". Experimental and Therapeutic Medicine 17, no. 1 (2019): 613-620. https://doi.org/10.3892/etm.2018.7007
Copy and paste a formatted citation
x
Spandidos Publications style
Ju Y, Sun C and Wang X: Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma. Exp Ther Med 17: 613-620, 2019.
APA
Ju, Y., Sun, C., & Wang, X. (2019). Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma. Experimental and Therapeutic Medicine, 17, 613-620. https://doi.org/10.3892/etm.2018.7007
MLA
Ju, Y., Sun, C., Wang, X."Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma". Experimental and Therapeutic Medicine 17.1 (2019): 613-620.
Chicago
Ju, Y., Sun, C., Wang, X."Loss of atypical chemokine receptor 4 facilitates C‑C motif chemokine ligand 21‑mediated tumor growth and invasion in nasopharyngeal carcinoma". Experimental and Therapeutic Medicine 17, no. 1 (2019): 613-620. https://doi.org/10.3892/etm.2018.7007
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