4.6 Article

Overexpression of miR-155 promotes the proliferation and invasion of oral squamous carcinoma cells by regulating BCL6/cyclin D2

Journal

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume 37, Issue 5, Pages 1274-1280

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2016.2529

Keywords

miR-155; oral squamous cell carcinoma; proliferation; migration; invasion; B-cell CLL/lymphoma 6; cyclin D2

Funding

  1. National Natural Science Foundation of China [81272948, 81000446]
  2. Specialized Research Fund for the Doctoral Program of Higher Education of China [201001711201050]
  3. Provincial Natural Scientific Foundation of Guangdong [10451008901005050]
  4. Guangdong Department of Science and Technology Translational Medicine Center Grant [2011A080300002]
  5. Priming Scientific Research Foundation [10ykpy17]

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Although microRNA-155 (miR-155) is known to play an important role in many cancers, its expression and function in oral squamous cell carcinoma (OSCC) was not fully understood. Thus, in the present study, we investigated the expression of miR-155 and also the role this miR plays in OSCC. We used the OSCC cell line (CAL27) and paired tumor and non-tumor tissue samples from patients with OSCC in order to detect the expression of miR-155. Cell proliferation, migration and invasion assays were then undertaken in order to determine the effect of miR-155 on the biological behavior of CAL27 cells following transient transfection with miR-155 mimic and antagomir. The regulatory effect of miR-155 on its target gene B-cell CLL/lymphoma 6 (BCL6) and downstream gene cyclin D2 (CCND2) was also analyzed. We found that miR-155 expression in OSCC cell and tumor tissues was significantly higher than that of the controls. We noted that the miR-155 mimic enhanced CAL27 cell proliferation, migration and invasion ability, downregulated BCL6 levels, and increased cyclin D2 expression. However, we noted that abrogating miR-155 with the miR-155 antagomir suppressed CAL27 cell proliferation, migration and invasion, upregulated BCL6 and reduced cyclin D2 expression. These results indicate that miR-155 plays a tumor-promoting role in OSCC by regulating the BCL6/cyclin D2 axis.

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