Loss of atypical chemokine receptor 4 facilitates C-C motif chemokine ligand 21-mediated tumor growth and invasion in nasopharyngeal carcinoma
| Autor: | Xiaoli Wang, Yunhe Ju, Chuanzheng Sun |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Chemokine endocrine system growth 03 medical and health sciences 0302 clinical medicine Atypical Chemokine Receptor 4 Immunology and Microbiology (miscellaneous) medicine otorhinolaryngologic diseases metastasis atypical chemokine receptor Gene knockdown biology Oncogene nasopharyngeal carcinoma General Medicine Articles Cell cycle medicine.disease invasion stomatognathic diseases 030104 developmental biology Nasopharyngeal carcinoma 030220 oncology & carcinogenesis Cancer research biology.protein CCL25 CCL21 |
| Zdroj: | Experimental and Therapeutic Medicine |
| ISSN: | 1792-0981 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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