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MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma
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 exp...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166217/ https://www.ncbi.nlm.nih.gov/pubmed/25246801 http://dx.doi.org/10.2147/OTT.S67624 |
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author | Lin, Feiou Yao, Linjie Xiao, Jin Liu, DengFeng Ni, Zhenyu |
author_facet | Lin, Feiou Yao, Linjie Xiao, Jin Liu, DengFeng Ni, Zhenyu |
author_sort | Lin, Feiou |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4166217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-41662172014-09-22 MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma Lin, Feiou Yao, Linjie Xiao, Jin Liu, DengFeng Ni, Zhenyu Onco Targets Ther Original Research 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. Dove Medical Press 2014-09-11 /pmc/articles/PMC4166217/ /pubmed/25246801 http://dx.doi.org/10.2147/OTT.S67624 Text en © 2014 Lin et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Lin, Feiou Yao, Linjie Xiao, Jin Liu, DengFeng Ni, Zhenyu MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title | MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title_full | MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title_fullStr | MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title_full_unstemmed | MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title_short | MiR-206 functions as a tumor suppressor and directly targets K-Ras in human oral squamous cell carcinoma |
title_sort | mir-206 functions as a tumor suppressor and directly targets k-ras in human oral squamous cell carcinoma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166217/ https://www.ncbi.nlm.nih.gov/pubmed/25246801 http://dx.doi.org/10.2147/OTT.S67624 |
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