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Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is the major histological type of esophageal cancer in developing countries. The prognosis and survival rate of ESCC are very poor. Recently, microRNAs (miRNAs) have emerged as important regulators of cancer cell biological processes. To better u...

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Autores principales: Li, Heping, Zheng, Dayong, Zhang, Bing, Liu, Liangshuai, Ou, Junwei, Chen, Wei, Xiong, Shiqiu, Gu, Yong, Yang, Jianyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107867/
https://www.ncbi.nlm.nih.gov/pubmed/25023649
http://dx.doi.org/10.1186/1479-5876-12-196
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author Li, Heping
Zheng, Dayong
Zhang, Bing
Liu, Liangshuai
Ou, Junwei
Chen, Wei
Xiong, Shiqiu
Gu, Yong
Yang, Jianyong
author_facet Li, Heping
Zheng, Dayong
Zhang, Bing
Liu, Liangshuai
Ou, Junwei
Chen, Wei
Xiong, Shiqiu
Gu, Yong
Yang, Jianyong
author_sort Li, Heping
collection PubMed
description BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is the major histological type of esophageal cancer in developing countries. The prognosis and survival rate of ESCC are very poor. Recently, microRNAs (miRNAs) have emerged as important regulators of cancer cell biological processes. To better understanding the molecular mechanisms by which they regulate the behavior of cancer cells is needed. METHODS: The expression of miR-208 was examined in ESCC cell lines and tumor tissues by real-time PCR. Proliferation capability of ESCC cells upon regulation of miR-208 expression was detected by MTT assay, colony formation assay, anchorage-independent growth ability assay and flow cytometry analysis. The target of miR-208 was determined by western blotting analysis, luciferase reporter assay and real-time PCR. RESULTS: miR-208 was upregulated in ESCC cell lines and tissues. Overexpression of miR-208 in ESCC cells increased cell proliferation, tumorigenicity and cell cycle progression, whereas inhibition of miR-208 reduced cells proliferation, tumorigenicity and cell cycle progression. Additionally, SOX6 was identified as a direct target of miR-208. Ectopic expression of miR-208 led to downregulation of SOX6 protein, which resulted in the downregulation of p21, upregulation of cyclin D1 and phosphorylation of Rb. CONCLUSIONS: These results suggest that miR-208 represents a potential onco-miR and participates in ESCC carcinogenesis by suppressing SOX6 expression.
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spelling pubmed-41078672014-07-24 Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma Li, Heping Zheng, Dayong Zhang, Bing Liu, Liangshuai Ou, Junwei Chen, Wei Xiong, Shiqiu Gu, Yong Yang, Jianyong J Transl Med Research BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is the major histological type of esophageal cancer in developing countries. The prognosis and survival rate of ESCC are very poor. Recently, microRNAs (miRNAs) have emerged as important regulators of cancer cell biological processes. To better understanding the molecular mechanisms by which they regulate the behavior of cancer cells is needed. METHODS: The expression of miR-208 was examined in ESCC cell lines and tumor tissues by real-time PCR. Proliferation capability of ESCC cells upon regulation of miR-208 expression was detected by MTT assay, colony formation assay, anchorage-independent growth ability assay and flow cytometry analysis. The target of miR-208 was determined by western blotting analysis, luciferase reporter assay and real-time PCR. RESULTS: miR-208 was upregulated in ESCC cell lines and tissues. Overexpression of miR-208 in ESCC cells increased cell proliferation, tumorigenicity and cell cycle progression, whereas inhibition of miR-208 reduced cells proliferation, tumorigenicity and cell cycle progression. Additionally, SOX6 was identified as a direct target of miR-208. Ectopic expression of miR-208 led to downregulation of SOX6 protein, which resulted in the downregulation of p21, upregulation of cyclin D1 and phosphorylation of Rb. CONCLUSIONS: These results suggest that miR-208 represents a potential onco-miR and participates in ESCC carcinogenesis by suppressing SOX6 expression. BioMed Central 2014-07-15 /pmc/articles/PMC4107867/ /pubmed/25023649 http://dx.doi.org/10.1186/1479-5876-12-196 Text en Copyright © 2014 Li et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Li, Heping
Zheng, Dayong
Zhang, Bing
Liu, Liangshuai
Ou, Junwei
Chen, Wei
Xiong, Shiqiu
Gu, Yong
Yang, Jianyong
Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title_full Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title_fullStr Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title_full_unstemmed Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title_short Mir-208 promotes cell proliferation by repressing SOX6 expression in human esophageal squamous cell carcinoma
title_sort mir-208 promotes cell proliferation by repressing sox6 expression in human esophageal squamous cell carcinoma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107867/
https://www.ncbi.nlm.nih.gov/pubmed/25023649
http://dx.doi.org/10.1186/1479-5876-12-196
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