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microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein
Oral squamous cell carcinoma (OSCC), the most common pathological type of oral cancer, is still a frequent malignancy with unsatisfactory prognosis. Accumulating studies have proven some microRNAs (miRNAs) can function as oncogenes in OSCC by targeting tumor suppressors. In this study, we first inve...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585605/ https://www.ncbi.nlm.nih.gov/pubmed/30260023 http://dx.doi.org/10.1002/jcb.27753 |
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author | Zheng, Jiabao Wang, Jiali Jia, Yunlong Liu, Tianxu Duan, Yuqing Liang, Xing Liu, Lihua |
author_facet | Zheng, Jiabao Wang, Jiali Jia, Yunlong Liu, Tianxu Duan, Yuqing Liang, Xing Liu, Lihua |
author_sort | Zheng, Jiabao |
collection | PubMed |
description | Oral squamous cell carcinoma (OSCC), the most common pathological type of oral cancer, is still a frequent malignancy with unsatisfactory prognosis. Accumulating studies have proven some microRNAs (miRNAs) can function as oncogenes in OSCC by targeting tumor suppressors. In this study, we first investigated the expression and role of tumor suppressor bridging integrator‐1 (BIN1) in OSCC tissues and cells. Our results indicated that BIN1 was low expressed in the OSCC tissues and cell lines (SCC6, SCC9, SCC25, HN4, and HN6) along with miR‐211 was highly expressed in OSCC tissues and cell lines, and BIN1 overexpression could evidently inhibit their proliferation, migration, and invasion abilities. Next, we used bioinformation algorithms to predict the potential miRNA targeting BIN1 and chose miR‐211 for further study. miR‐211, a highly expressed miRNA in OSCC cells, could specifically bind with the 3′‐untranslated region (3′‐UTR) of BIN1 to trigger its degradation. Addition of miR‐211 inhibitor could evidently suppress the malignant behaviors of OSCC cells by upregulating BIN1 expression and inhibit the activation of the EGFR/MAPK pathway. Taken together the findings of the study indicated that miR‐211 mediated BIN1 downregulation had crucial significances in OSCC, suggesting the miR‐211 might be a novel potential therapeutic target for the OSCC treatment. |
format | Online Article Text |
id | pubmed-6585605 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-65856052019-06-27 microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein Zheng, Jiabao Wang, Jiali Jia, Yunlong Liu, Tianxu Duan, Yuqing Liang, Xing Liu, Lihua J Cell Biochem Research Articles Oral squamous cell carcinoma (OSCC), the most common pathological type of oral cancer, is still a frequent malignancy with unsatisfactory prognosis. Accumulating studies have proven some microRNAs (miRNAs) can function as oncogenes in OSCC by targeting tumor suppressors. In this study, we first investigated the expression and role of tumor suppressor bridging integrator‐1 (BIN1) in OSCC tissues and cells. Our results indicated that BIN1 was low expressed in the OSCC tissues and cell lines (SCC6, SCC9, SCC25, HN4, and HN6) along with miR‐211 was highly expressed in OSCC tissues and cell lines, and BIN1 overexpression could evidently inhibit their proliferation, migration, and invasion abilities. Next, we used bioinformation algorithms to predict the potential miRNA targeting BIN1 and chose miR‐211 for further study. miR‐211, a highly expressed miRNA in OSCC cells, could specifically bind with the 3′‐untranslated region (3′‐UTR) of BIN1 to trigger its degradation. Addition of miR‐211 inhibitor could evidently suppress the malignant behaviors of OSCC cells by upregulating BIN1 expression and inhibit the activation of the EGFR/MAPK pathway. Taken together the findings of the study indicated that miR‐211 mediated BIN1 downregulation had crucial significances in OSCC, suggesting the miR‐211 might be a novel potential therapeutic target for the OSCC treatment. John Wiley and Sons Inc. 2018-09-27 2019-03 /pmc/articles/PMC6585605/ /pubmed/30260023 http://dx.doi.org/10.1002/jcb.27753 Text en © 2018 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by-n/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Zheng, Jiabao Wang, Jiali Jia, Yunlong Liu, Tianxu Duan, Yuqing Liang, Xing Liu, Lihua microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title | microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title_full | microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title_fullStr | microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title_full_unstemmed | microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title_short | microRNA‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
title_sort | microrna‐211 promotes proliferation, migration, and invasion ability of oral squamous cell carcinoma cells via targeting the bridging integrator 1 protein |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585605/ https://www.ncbi.nlm.nih.gov/pubmed/30260023 http://dx.doi.org/10.1002/jcb.27753 |
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