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Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5

Hepatocellular carcinoma has been identified as the fifth most common cancer in men and the ninth in women worldwide. Despite many efforts have been made in recent years, the overall survival rate of patients with hepatocellular carcinoma still remain unsatisfied. Therefore, exploring the mechanisms...

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Autores principales: Liu, Bin, Li, Jing, Liu, Xiaoling, Zheng, Min, Yang, Ye, Lyu, Qian, Jin, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752538/
https://www.ncbi.nlm.nih.gov/pubmed/29312625
http://dx.doi.org/10.18632/oncotarget.22723
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author Liu, Bin
Li, Jing
Liu, Xiaoling
Zheng, Min
Yang, Ye
Lyu, Qian
Jin, Li
author_facet Liu, Bin
Li, Jing
Liu, Xiaoling
Zheng, Min
Yang, Ye
Lyu, Qian
Jin, Li
author_sort Liu, Bin
collection PubMed
description Hepatocellular carcinoma has been identified as the fifth most common cancer in men and the ninth in women worldwide. Despite many efforts have been made in recent years, the overall survival rate of patients with hepatocellular carcinoma still remain unsatisfied. Therefore, exploring the mechanisms underlying the progression of hepatocellular carcinoma is essential for developing novel treatments to improve patient prognosis. HOXA11-AS, transcribed from the opposite strand of the protein-coding gene HOXA11, has been identified to be associated with the malignant characteristics of several cancers. However, the biological role and molecular mechanism of HOXA11-AS in hepatocellular carcinoma still need to be further investigated. In the current study, the expression of HOXA11-AS in the hepatocellular carcinoma cell lines and tissues was measured by quantitative real-time PCR. Loss-of-function and gain-of-function approaches were applied to investigate the proliferative function of HOXA11-AS in hepatocellular carcinoma cells. Results from flow cytometric analysis of apoptosis and cell cycle distribution revealed that HOXA11-AS promoted hepatocellular carcinoma cells proliferation through regulating cell cycle and apoptosis. Gene chip technology and quantitative real-time PCR confirmed that DUSP5 was a downstream target of HOXA11-AS. RNA immune co-precipitation assays, RNA pull-down and Chromatin immunoprecipitation assays confirmed that HOXA11-AS could recruit EZH2 to the promoter region of DUSP5, which therefore suppressed the transcription of DUSP5. Collectively, these findings revealed that HOXA11-AS functions as an oncogene in hepatocellular carcinoma through interacting with polycomb-repressive complex2.
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spelling pubmed-57525382018-01-08 Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5 Liu, Bin Li, Jing Liu, Xiaoling Zheng, Min Yang, Ye Lyu, Qian Jin, Li Oncotarget Research Paper Hepatocellular carcinoma has been identified as the fifth most common cancer in men and the ninth in women worldwide. Despite many efforts have been made in recent years, the overall survival rate of patients with hepatocellular carcinoma still remain unsatisfied. Therefore, exploring the mechanisms underlying the progression of hepatocellular carcinoma is essential for developing novel treatments to improve patient prognosis. HOXA11-AS, transcribed from the opposite strand of the protein-coding gene HOXA11, has been identified to be associated with the malignant characteristics of several cancers. However, the biological role and molecular mechanism of HOXA11-AS in hepatocellular carcinoma still need to be further investigated. In the current study, the expression of HOXA11-AS in the hepatocellular carcinoma cell lines and tissues was measured by quantitative real-time PCR. Loss-of-function and gain-of-function approaches were applied to investigate the proliferative function of HOXA11-AS in hepatocellular carcinoma cells. Results from flow cytometric analysis of apoptosis and cell cycle distribution revealed that HOXA11-AS promoted hepatocellular carcinoma cells proliferation through regulating cell cycle and apoptosis. Gene chip technology and quantitative real-time PCR confirmed that DUSP5 was a downstream target of HOXA11-AS. RNA immune co-precipitation assays, RNA pull-down and Chromatin immunoprecipitation assays confirmed that HOXA11-AS could recruit EZH2 to the promoter region of DUSP5, which therefore suppressed the transcription of DUSP5. Collectively, these findings revealed that HOXA11-AS functions as an oncogene in hepatocellular carcinoma through interacting with polycomb-repressive complex2. Impact Journals LLC 2017-11-27 /pmc/articles/PMC5752538/ /pubmed/29312625 http://dx.doi.org/10.18632/oncotarget.22723 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liu, Bin
Li, Jing
Liu, Xiaoling
Zheng, Min
Yang, Ye
Lyu, Qian
Jin, Li
Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title_full Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title_fullStr Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title_full_unstemmed Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title_short Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5
title_sort long non-coding rna hoxa11-as promotes the proliferation hcc cells by epigenetically silencing dusp5
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5752538/
https://www.ncbi.nlm.nih.gov/pubmed/29312625
http://dx.doi.org/10.18632/oncotarget.22723
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