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Function of low ADARB1 expression in lung adenocarcinoma

Adenosine deaminase RNA-specific B1 (ADARB1), an adenosine-to-inosine (A-to-I) RNA-editing enzyme, has been found to play an essential role in the development of cancer. However, the specific function of ADARB1 in lung cancer, especially in lung adenocarcinoma (LUAD), is still not fully understood a...

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Autores principales: Wang, Xiang, Xu, Zhijie, Ren, Xinxin, Chen, Xi, Wei, Jie, Lin, Wei, Li, Zhi, Ou, Chunlin, Gong, Zhicheng, Yan, Yuanliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6730894/
https://www.ncbi.nlm.nih.gov/pubmed/31491024
http://dx.doi.org/10.1371/journal.pone.0222298
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author Wang, Xiang
Xu, Zhijie
Ren, Xinxin
Chen, Xi
Wei, Jie
Lin, Wei
Li, Zhi
Ou, Chunlin
Gong, Zhicheng
Yan, Yuanliang
author_facet Wang, Xiang
Xu, Zhijie
Ren, Xinxin
Chen, Xi
Wei, Jie
Lin, Wei
Li, Zhi
Ou, Chunlin
Gong, Zhicheng
Yan, Yuanliang
author_sort Wang, Xiang
collection PubMed
description Adenosine deaminase RNA-specific B1 (ADARB1), an adenosine-to-inosine (A-to-I) RNA-editing enzyme, has been found to play an essential role in the development of cancer. However, the specific function of ADARB1 in lung cancer, especially in lung adenocarcinoma (LUAD), is still not fully understood and requires further study. In our study, integrative bioinformatics were used to analyze the detailed function of ADARB1 in LUAD. By conducting bioinformatics analyses of several public databases, such as Gene Expression Profiling Interactive Analysis (GEPIA), GE-mini, and Oncomine, we found significantly decreased ADARB1 expression in LUAD cells and tissues. Moreover, RT-PCR and Western blot showed lower ADARB1 expression in H358 and A549 LUAD cells compared to human bronchial epithelial Beas-2B cells. Wound Healing Assay indicated that knockdown ADARB1 could promote LUAD cell metastasis. By using the Kaplan-Meier Plotter tool, we found that downregulation of ADARB1 was related to shorter first progression (FP), overall survival time (OS) and post-progression survival time (PPS). The relevant clinical data acquired from the Wanderer database indicated that the expression and methylation values of ADARB1 were significantly associated with the clinical characteristics of LUAD. Using DNA methylation inhibitor, we found DNMT inhibitor 5-aza-2-deoxycytidine (5-azaD) could promote the expression of ADARB1 and reverse the inhibition effect of ADARB1 in migration. In addition, functional enrichment analysis of ADARB1-associated coexpression genes was further conducted. Our investigation demonstrated that low levels of ADARB1 were specifically found in LUAD, and this gene might be a potential target in the diagnostic and prognostic evaluation of LUAD patients.
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spelling pubmed-67308942019-09-16 Function of low ADARB1 expression in lung adenocarcinoma Wang, Xiang Xu, Zhijie Ren, Xinxin Chen, Xi Wei, Jie Lin, Wei Li, Zhi Ou, Chunlin Gong, Zhicheng Yan, Yuanliang PLoS One Research Article Adenosine deaminase RNA-specific B1 (ADARB1), an adenosine-to-inosine (A-to-I) RNA-editing enzyme, has been found to play an essential role in the development of cancer. However, the specific function of ADARB1 in lung cancer, especially in lung adenocarcinoma (LUAD), is still not fully understood and requires further study. In our study, integrative bioinformatics were used to analyze the detailed function of ADARB1 in LUAD. By conducting bioinformatics analyses of several public databases, such as Gene Expression Profiling Interactive Analysis (GEPIA), GE-mini, and Oncomine, we found significantly decreased ADARB1 expression in LUAD cells and tissues. Moreover, RT-PCR and Western blot showed lower ADARB1 expression in H358 and A549 LUAD cells compared to human bronchial epithelial Beas-2B cells. Wound Healing Assay indicated that knockdown ADARB1 could promote LUAD cell metastasis. By using the Kaplan-Meier Plotter tool, we found that downregulation of ADARB1 was related to shorter first progression (FP), overall survival time (OS) and post-progression survival time (PPS). The relevant clinical data acquired from the Wanderer database indicated that the expression and methylation values of ADARB1 were significantly associated with the clinical characteristics of LUAD. Using DNA methylation inhibitor, we found DNMT inhibitor 5-aza-2-deoxycytidine (5-azaD) could promote the expression of ADARB1 and reverse the inhibition effect of ADARB1 in migration. In addition, functional enrichment analysis of ADARB1-associated coexpression genes was further conducted. Our investigation demonstrated that low levels of ADARB1 were specifically found in LUAD, and this gene might be a potential target in the diagnostic and prognostic evaluation of LUAD patients. Public Library of Science 2019-09-06 /pmc/articles/PMC6730894/ /pubmed/31491024 http://dx.doi.org/10.1371/journal.pone.0222298 Text en © 2019 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Wang, Xiang
Xu, Zhijie
Ren, Xinxin
Chen, Xi
Wei, Jie
Lin, Wei
Li, Zhi
Ou, Chunlin
Gong, Zhicheng
Yan, Yuanliang
Function of low ADARB1 expression in lung adenocarcinoma
title Function of low ADARB1 expression in lung adenocarcinoma
title_full Function of low ADARB1 expression in lung adenocarcinoma
title_fullStr Function of low ADARB1 expression in lung adenocarcinoma
title_full_unstemmed Function of low ADARB1 expression in lung adenocarcinoma
title_short Function of low ADARB1 expression in lung adenocarcinoma
title_sort function of low adarb1 expression in lung adenocarcinoma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6730894/
https://www.ncbi.nlm.nih.gov/pubmed/31491024
http://dx.doi.org/10.1371/journal.pone.0222298
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