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Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) remains one of the most common types of cancer worldwide and prognosis remains poor. Previous studies have suggested that long non-coding RNAs (lncRNAs) may be key regulators of tumor development and progression in HCC. It has been determined that 61–72% of transcribed...

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Autores principales: Lan, Tian, Chang, Lei, Wu, Long, Yuan, Yufeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102020/
https://www.ncbi.nlm.nih.gov/pubmed/27748842
http://dx.doi.org/10.3892/mmr.2016.5836
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author Lan, Tian
Chang, Lei
Wu, Long
Yuan, Yufeng
author_facet Lan, Tian
Chang, Lei
Wu, Long
Yuan, Yufeng
author_sort Lan, Tian
collection PubMed
description Hepatocellular carcinoma (HCC) remains one of the most common types of cancer worldwide and prognosis remains poor. Previous studies have suggested that long non-coding RNAs (lncRNAs) may be key regulators of tumor development and progression in HCC. It has been determined that 61–72% of transcribed regions contain lncRNAs in the antisense orientation (aslncRNAs). However, the function of aslncRNAs in HCC remains to be elucidated. The present study investigated the function of the aslncRNA zinc finger E-box binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in 40 HCC tissues and 5 different human HCC cell lines using reverse transcription-quantitative polymerase chain reaction. Additionally, the expression levels of ZEB2-AS1 were downregulated by transfection of small interfering RNAs (siRNAs) to determine whether ZEB2-AS1 is capable of affecting cell proliferation, invasion and metastasis by regulating ZEB2, vimentin, fibronectin, E-cadherin and N-cadherin expression levels. The results of the present study demonstrated that the expression levels of ZEB2-AS1 were greater in HCC tissues when compared with the adjacent normal tissues. Furthermore, ZEB2-AS1 expression was significantly associated with the size of the primary tumor, intrahepatic metastasis and tumor-node-metastasis stage. The Kaplan-Meier survival curves suggested that patients with high ZEB2-AS1 expression levels experienced the lowest overall and recurrence-free survival rates compared with those that had low expression levels. In addition, the current study demonstrated that the downregulation of ZEB2-AS1 was associated with decreased tumor growth and metastasis in HCC by the regulation of the expression levels of epithelial mesenchymal transition-induced markers. In conclusion, lncRNA ZEB2-AS1 may be used as a valuable biomarker in patients with HCC.
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spelling pubmed-51020202016-11-22 Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma Lan, Tian Chang, Lei Wu, Long Yuan, Yufeng Mol Med Rep Articles Hepatocellular carcinoma (HCC) remains one of the most common types of cancer worldwide and prognosis remains poor. Previous studies have suggested that long non-coding RNAs (lncRNAs) may be key regulators of tumor development and progression in HCC. It has been determined that 61–72% of transcribed regions contain lncRNAs in the antisense orientation (aslncRNAs). However, the function of aslncRNAs in HCC remains to be elucidated. The present study investigated the function of the aslncRNA zinc finger E-box binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in 40 HCC tissues and 5 different human HCC cell lines using reverse transcription-quantitative polymerase chain reaction. Additionally, the expression levels of ZEB2-AS1 were downregulated by transfection of small interfering RNAs (siRNAs) to determine whether ZEB2-AS1 is capable of affecting cell proliferation, invasion and metastasis by regulating ZEB2, vimentin, fibronectin, E-cadherin and N-cadherin expression levels. The results of the present study demonstrated that the expression levels of ZEB2-AS1 were greater in HCC tissues when compared with the adjacent normal tissues. Furthermore, ZEB2-AS1 expression was significantly associated with the size of the primary tumor, intrahepatic metastasis and tumor-node-metastasis stage. The Kaplan-Meier survival curves suggested that patients with high ZEB2-AS1 expression levels experienced the lowest overall and recurrence-free survival rates compared with those that had low expression levels. In addition, the current study demonstrated that the downregulation of ZEB2-AS1 was associated with decreased tumor growth and metastasis in HCC by the regulation of the expression levels of epithelial mesenchymal transition-induced markers. In conclusion, lncRNA ZEB2-AS1 may be used as a valuable biomarker in patients with HCC. D.A. Spandidos 2016-11 2016-10-12 /pmc/articles/PMC5102020/ /pubmed/27748842 http://dx.doi.org/10.3892/mmr.2016.5836 Text en Copyright: © Lan et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lan, Tian
Chang, Lei
Wu, Long
Yuan, Yufeng
Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title_full Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title_fullStr Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title_full_unstemmed Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title_short Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma
title_sort downregulation of zeb2-as1 decreased tumor growth and metastasis in hepatocellular carcinoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102020/
https://www.ncbi.nlm.nih.gov/pubmed/27748842
http://dx.doi.org/10.3892/mmr.2016.5836
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