MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma
This paper has been retracted
Feiou Lin,1 Linjie Yao,2 Jin Xiao,3 DengFeng Liu,3 Zhenyu Ni1
1Department of Orthodontics, 2Department of Pedodontics, 3Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, People’s Republic of China
Purpose: MicroRNA-206 (miR-206) has been proven to be downregulated in many human malignancies and is correlated with tumor progression. However, the roles of miR-206 and its related molecular mechanisms in oral squamous cell carcinoma (OSCC) are still unclear. Thus, the aim of this study was to explore the effects of miR-206 in OSCC tumorigenesis and development.
Methods: Quantitative real-time polymerase chain reaction was used to detect miR-206 expression in OSCC cell lines and primary tumor tissues. The association of miR-206 expression with clinicopathological factors and prognosis was also analyzed. In addition, the effects of miR-206 on the biological behavior of OSCC cells were investigated. Lastly, the potential regulatory function of miR-206 on K-Ras expression was confirmed.
Results: MiR-206 expression was significantly downregulated in OSCC tissue samples and cell lines (both P<0.001). Decreased miR-206 expression was significantly associated with advanced tumor node metastasis (TNM) stage, advanced T classifications (ie, size and/or extent of the primary tumor), positive N classification (ie, spread to regional lymph nodes), and shorter overall survival. In addition, upregulation of miR-206 in Tca8113 cells was able to reduce cell proliferation, invasion, and migration and promote cell apoptosis in vitro. Further, K-Ras was confirmed as a direct target of miR-206 by using luciferase reporter assay.
Conclusion: These findings indicate that miR-206 may act as a tumor suppressor in OSCC and could serve as a novel therapeutic agent for miR-based therapy.
Keywords: miR-206, oral squamous cell carcinoma, prognosis, proliferation, apoptosis, invasion
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