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Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation

Adenosine (A) to inosine (I) RNA editing is the most prevalent RNA editing mechanism in humans and plays critical roles in tumorigenesis. However, the effects of radiation on RNA editing were poorly understood, and a deeper understanding of the radiation-induced cancer is imperative. Here, we analyz...

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Autores principales: Liu, Qiaowei, Li, Hao, You, Lukuan, Li, Tao, Li, Lingling, Zhou, Pingkun, Bo, Xiaochen, Chen, Hebing, Chen, Xiaohua, Hu, Yi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546236/
https://www.ncbi.nlm.nih.gov/pubmed/31158229
http://dx.doi.org/10.1371/journal.pone.0213047
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author Liu, Qiaowei
Li, Hao
You, Lukuan
Li, Tao
Li, Lingling
Zhou, Pingkun
Bo, Xiaochen
Chen, Hebing
Chen, Xiaohua
Hu, Yi
author_facet Liu, Qiaowei
Li, Hao
You, Lukuan
Li, Tao
Li, Lingling
Zhou, Pingkun
Bo, Xiaochen
Chen, Hebing
Chen, Xiaohua
Hu, Yi
author_sort Liu, Qiaowei
collection PubMed
description Adenosine (A) to inosine (I) RNA editing is the most prevalent RNA editing mechanism in humans and plays critical roles in tumorigenesis. However, the effects of radiation on RNA editing were poorly understood, and a deeper understanding of the radiation-induced cancer is imperative. Here, we analyzed BEP2D (a human bronchial epithelial cell line) and radiation-induced malignantly transformed cell lines with next generation sequencing. By performing an integrated analysis of A-to-I RNA editing, we found that single-nucleotide variants (SNVs) might induce the downregulation of ADAR2 enzymes, and further caused the abnormal occurrence of RNA editing in malignantly transformed cell lines. These editing events were significantly enriched in differentially expressed genes between normal cell line and malignantly transformed cell lines. In addition, oncogenes CTNNB1 and FN1 were highly edited and significantly overexpressed in malignantly transformed cell lines, thus may be responsible for the lung cancer progression. Our work provides a systematic analysis of RNA editing from cell lines derived from human bronchial epithelial cells with high-throughput RNA sequencing and DNA sequencing. Moreover, these results provide further evidence for RNA editing as an important tumorigenesis mechanism.
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spelling pubmed-65462362019-06-17 Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation Liu, Qiaowei Li, Hao You, Lukuan Li, Tao Li, Lingling Zhou, Pingkun Bo, Xiaochen Chen, Hebing Chen, Xiaohua Hu, Yi PLoS One Research Article Adenosine (A) to inosine (I) RNA editing is the most prevalent RNA editing mechanism in humans and plays critical roles in tumorigenesis. However, the effects of radiation on RNA editing were poorly understood, and a deeper understanding of the radiation-induced cancer is imperative. Here, we analyzed BEP2D (a human bronchial epithelial cell line) and radiation-induced malignantly transformed cell lines with next generation sequencing. By performing an integrated analysis of A-to-I RNA editing, we found that single-nucleotide variants (SNVs) might induce the downregulation of ADAR2 enzymes, and further caused the abnormal occurrence of RNA editing in malignantly transformed cell lines. These editing events were significantly enriched in differentially expressed genes between normal cell line and malignantly transformed cell lines. In addition, oncogenes CTNNB1 and FN1 were highly edited and significantly overexpressed in malignantly transformed cell lines, thus may be responsible for the lung cancer progression. Our work provides a systematic analysis of RNA editing from cell lines derived from human bronchial epithelial cells with high-throughput RNA sequencing and DNA sequencing. Moreover, these results provide further evidence for RNA editing as an important tumorigenesis mechanism. Public Library of Science 2019-06-03 /pmc/articles/PMC6546236/ /pubmed/31158229 http://dx.doi.org/10.1371/journal.pone.0213047 Text en © 2019 Liu 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
Liu, Qiaowei
Li, Hao
You, Lukuan
Li, Tao
Li, Lingling
Zhou, Pingkun
Bo, Xiaochen
Chen, Hebing
Chen, Xiaohua
Hu, Yi
Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title_full Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title_fullStr Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title_full_unstemmed Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title_short Genome-wide identification and analysis of A-to-I RNA editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
title_sort genome-wide identification and analysis of a-to-i rna editing events in the malignantly transformed cell lines from bronchial epithelial cell line induced by α-particles radiation
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546236/
https://www.ncbi.nlm.nih.gov/pubmed/31158229
http://dx.doi.org/10.1371/journal.pone.0213047
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