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Article

Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells

  • Authors:
    • Xiaofeng Wang
    • Jinting He
    • Xiaoming Zhao
    • Tianyang Qi
    • Tianfu Zhang
    • Chenfei Kong
  • View Affiliations / Copyright

    Affiliations: Department of Stomatology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Department of Neurology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Scientific Research Center, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China
  • Pages: 1835-1842
    |
    Published online on: February 14, 2018
       https://doi.org/10.3892/or.2018.6271
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Abstract

Epithelial-mesenchymal transition (EMT) is one of the major processes that contribute to the occurrence of cancer metastasis. EMT has been associated with the development of oral cancer. Syndecan‑1 (SDC1) is a key cell‑surface adhesion molecule and its expression level inversely correlates with tumor differentiation and prognosis. In the present study, we aimed to determine the role of SDC1 in oral cancer progression and investigate the molecular mechanisms through which SDC1 regulates the EMT and invasiveness of oral cancer cells. We demonstrated that basal SDC1 expression levels were lower in four oral cancer cell lines (KB, Tca8113, ACC2 and CAL‑27), than in normal human periodontal ligament fibroblasts. Ectopic overexpression of SDC1 resulted in morphological transformation, decreased expression of EMT‑associated markers, as well as decreased migration, invasiveness and proliferation of oral cancer cells. In contrast, downregulation of the expression of SDC1 caused the opposite results. Furthermore, the knockdown of endogenous SDC1 activated the extracellular signal‑regulated kinase (ERK) cascade, upregulated the expression of Snail and inhibited the expression of E‑cadherin. In conclusion, our findings revealed that SDC1 suppressed EMT via the modulation of the ERK signaling pathway that, in turn, negatively affected the invasiveness of human oral cancer cells. Our results provided useful evidence about the potential use of SDC1 as a molecular target for therapeutic interventions in human oral cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Wang X, He J, Zhao X, Qi T, Zhang T and Kong C: Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells. Oncol Rep 39: 1835-1842, 2018.
APA
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., & Kong, C. (2018). Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells. Oncology Reports, 39, 1835-1842. https://doi.org/10.3892/or.2018.6271
MLA
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., Kong, C."Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells". Oncology Reports 39.4 (2018): 1835-1842.
Chicago
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., Kong, C."Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells". Oncology Reports 39, no. 4 (2018): 1835-1842. https://doi.org/10.3892/or.2018.6271
Copy and paste a formatted citation
x
Spandidos Publications style
Wang X, He J, Zhao X, Qi T, Zhang T and Kong C: Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells. Oncol Rep 39: 1835-1842, 2018.
APA
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., & Kong, C. (2018). Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells. Oncology Reports, 39, 1835-1842. https://doi.org/10.3892/or.2018.6271
MLA
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., Kong, C."Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells". Oncology Reports 39.4 (2018): 1835-1842.
Chicago
Wang, X., He, J., Zhao, X., Qi, T., Zhang, T., Kong, C."Syndecan-1 suppresses epithelial-mesenchymal transition and migration in human oral cancer cells". Oncology Reports 39, no. 4 (2018): 1835-1842. https://doi.org/10.3892/or.2018.6271
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