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Article

Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma

  • Authors:
    • Xiao‑Peng Zhang
    • Zhi‑Juan Hu
    • Ai‑Hong Meng
    • Guo‑Chen Duan
    • Qing‑Tao Zhao
    • Jing Yang
  • View Affiliations / Copyright

    Affiliations: Department of Thoracic Surgery, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China, Department of Nephrology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China, Respiratory Division, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050050, P.R. China, Respiratory Division, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China
  • Pages: 8183-8189
    |
    Published online on: October 23, 2017
       https://doi.org/10.3892/ol.2017.7253
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Abstract

Previous studies have revealed that carcinoma‑associated fibroblasts communicate microenvironment-derived signals through chemokine/chemokine receptor interaction, resulting in carcinogenesis. C‑C motif chemokine ligand 20 (CCL20)/C‑C motif chemokine receptor 6 (CCR6) interactions are involved in the pathogenesis of colonic malignancies. The present study aimed to characterize the roles of CCL20/CCR6 and the extracellular signal‑regulated kinase (ERK) signaling pathway in lung adenocarcinoma growth. Lung adenocarcinoma samples obtained at surgery were assessed for the expression, tissue localization and production of CCL20/CCR6. In addition, colony formation, ERK signaling and chemokine production were measured to assess the responsiveness of the A549 cell line to CCL20 stimulation. CCL20 and CCR6 were found to be highly expressed in the majority of samples in the recurrence group (76 and 66%, respectively). The staining indexes of CCL20 and CCR6 in the recurrence group were 149.3 and 134.4, respectively, which were significantly higher than those in the non‑recurrence group (57.2 and 58.0, respectively); the protein and mRNA expression levels determined by western blot and reverse transcription‑quantitative polymerase chain reaction were also found to be high in the recurrence group For A549 cells, the colony‑forming capacity was increased by CCL20 stimulation, and this effect was dependent in part on ERK phosphorylation. Collectively, the findings suggest that CCR6 and CCL20 may serve a role in lung adenocarcinoma, leading to proliferation and migration via autocrine or paracrine mechanisms. The disruption of CCL20/CCR6 interactions may be a promising strategy for the treatment of cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang XP, Hu ZJ, Meng AH, Duan GC, Zhao QT and Yang J: Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma. Oncol Lett 14: 8183-8189, 2017.
APA
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., & Yang, J. (2017). Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma. Oncology Letters, 14, 8183-8189. https://doi.org/10.3892/ol.2017.7253
MLA
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., Yang, J."Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma". Oncology Letters 14.6 (2017): 8183-8189.
Chicago
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., Yang, J."Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma". Oncology Letters 14, no. 6 (2017): 8183-8189. https://doi.org/10.3892/ol.2017.7253
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang XP, Hu ZJ, Meng AH, Duan GC, Zhao QT and Yang J: Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma. Oncol Lett 14: 8183-8189, 2017.
APA
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., & Yang, J. (2017). Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma. Oncology Letters, 14, 8183-8189. https://doi.org/10.3892/ol.2017.7253
MLA
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., Yang, J."Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma". Oncology Letters 14.6 (2017): 8183-8189.
Chicago
Zhang, X., Hu, Z., Meng, A., Duan, G., Zhao, Q., Yang, J."Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma". Oncology Letters 14, no. 6 (2017): 8183-8189. https://doi.org/10.3892/ol.2017.7253
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