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Article

miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism

  • Authors:
    • Jing Cao
    • Tao Guo
    • Qingshan Dong
    • Jianqiang Zhang
    • Yanfeng Li
  • View Affiliations / Copyright

    Affiliations: Department of Stomatology, The First Affiliated Hospital of the PLA General Hospital, Beijing, P.R. China, Department of Stomatology, The Fifth Affiliated Hospital, Xinjiang Medical University, Urumqi, P.R. China, Department of Stomatology, Wuhan General Hospital of Guangzhou Command, People's Liberation Army, Wuhan, P.R. China
  • Pages: 974-980
    |
    Published online on: December 5, 2014
       https://doi.org/10.3892/or.2014.3648
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Abstract

MicroRNAs (miRNAs) are important gene regulators that play a profound role in tumorigenesis. Previous studies have revealed that miR-26b is downregulated in a wide range of malignant tumors and plays an important role in the regulation of carcinogenesis and tumor progression. In the present study, we revealed that miR-26b expression was decreased in human tongue squamous cell carcinoma and was associated with clinical stage, lymph node metastasis and survival prognosis. Ectopic expression of miR-26b suppressed the proliferation and metastasis of human tongue squamous cell carcinoma cells. Using a luciferase reporter assay, combined with western blot analysis results, we identified PTGS2 (prostaglandin-endoperoxide synthase-2, encoding COX-2) as the functional target of miR-26b. Specific inhibition of COX-2 activity by nimesulide further confirmed that miR-26b was able to regulate the cell proliferation and metastasis of the human tongue squamous cell carcinoma cells through a COX-2-dependent mechanism. Taken together, these results suggest that miR-26b serves as a tumor suppressor by targeting COX-2 and calls for the use of miR-26b as a potential therapeutic tool for human tongue squamous cell carcinoma, where COX-2 is often hyperactivated.
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Copy and paste a formatted citation
Spandidos Publications style
Cao J, Guo T, Dong Q, Zhang J and Li Y: miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism. Oncol Rep 33: 974-980, 2015.
APA
Cao, J., Guo, T., Dong, Q., Zhang, J., & Li, Y. (2015). miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism. Oncology Reports, 33, 974-980. https://doi.org/10.3892/or.2014.3648
MLA
Cao, J., Guo, T., Dong, Q., Zhang, J., Li, Y."miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism". Oncology Reports 33.2 (2015): 974-980.
Chicago
Cao, J., Guo, T., Dong, Q., Zhang, J., Li, Y."miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism". Oncology Reports 33, no. 2 (2015): 974-980. https://doi.org/10.3892/or.2014.3648
Copy and paste a formatted citation
x
Spandidos Publications style
Cao J, Guo T, Dong Q, Zhang J and Li Y: miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism. Oncol Rep 33: 974-980, 2015.
APA
Cao, J., Guo, T., Dong, Q., Zhang, J., & Li, Y. (2015). miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism. Oncology Reports, 33, 974-980. https://doi.org/10.3892/or.2014.3648
MLA
Cao, J., Guo, T., Dong, Q., Zhang, J., Li, Y."miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism". Oncology Reports 33.2 (2015): 974-980.
Chicago
Cao, J., Guo, T., Dong, Q., Zhang, J., Li, Y."miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism". Oncology Reports 33, no. 2 (2015): 974-980. https://doi.org/10.3892/or.2014.3648
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