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Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma

Euchromatic histone-lysine N-methyltransferase (G9A), the primary histone methyltransferase for histone H3 Lys(9), has been identified to be upregulated in numerous types of cancer. The aim of the present study was to analyze the clinical significance of G9A, and preliminarily explore its function i...

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Autores principales: Qin, Jian, Li, Qingyun, Zeng, Zhi, Wu, Ping, Jiang, Yanping, Luo, Tao, Ji, Xiang, Zhang, Qiuping, Hao, Yarong, Chen, Lang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004641/
https://www.ncbi.nlm.nih.gov/pubmed/29928350
http://dx.doi.org/10.3892/ol.2018.8572
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author Qin, Jian
Li, Qingyun
Zeng, Zhi
Wu, Ping
Jiang, Yanping
Luo, Tao
Ji, Xiang
Zhang, Qiuping
Hao, Yarong
Chen, Lang
author_facet Qin, Jian
Li, Qingyun
Zeng, Zhi
Wu, Ping
Jiang, Yanping
Luo, Tao
Ji, Xiang
Zhang, Qiuping
Hao, Yarong
Chen, Lang
author_sort Qin, Jian
collection PubMed
description Euchromatic histone-lysine N-methyltransferase (G9A), the primary histone methyltransferase for histone H3 Lys(9), has been identified to be upregulated in numerous types of cancer. The aim of the present study was to analyze the clinical significance of G9A, and preliminarily explore its function in hepatocellular carcinoma (HCC). An increased expression level of G9A was demonstrated in the HCC samples and also in 5 publically available datasets. By analyzing GSE14520, it was revealed that its expression level was significantly associated with serum α-fetoprotein level of patients with HCC, and may serve as a potential prognostic indicator for patients with multinodular HCC. Bioinformatics tools were utilized to predict the potential function of G9A, and the results indicated that G9A may modulate gene sets involved in RNA processing and DNA replication. G9A inhibition may suppress cell proliferation by arresting cells in G1 phase and increasing the expression level of microtubule-associated protein light chain 3β (MAP1LC3B) in Huh7 and HepG2 cells. In addition, an inverse association between the expression of G9A and LC3B was demonstrated in HCC tumor samples in the publically available GSE14520 dataset, which indicated that G9A may also have the potential to regulate MAP1LC3B expression in HCC tumor tissues. The results of the present study led to hypothesis that the G9A expression level may be of assistance in diagnosing HCC, and be a potential therapeutic target for HCC. The results provided novel evidence for additional understanding of the crucial role of G9A in tumorigenesis.
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spelling pubmed-60046412018-06-20 Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma Qin, Jian Li, Qingyun Zeng, Zhi Wu, Ping Jiang, Yanping Luo, Tao Ji, Xiang Zhang, Qiuping Hao, Yarong Chen, Lang Oncol Lett Articles Euchromatic histone-lysine N-methyltransferase (G9A), the primary histone methyltransferase for histone H3 Lys(9), has been identified to be upregulated in numerous types of cancer. The aim of the present study was to analyze the clinical significance of G9A, and preliminarily explore its function in hepatocellular carcinoma (HCC). An increased expression level of G9A was demonstrated in the HCC samples and also in 5 publically available datasets. By analyzing GSE14520, it was revealed that its expression level was significantly associated with serum α-fetoprotein level of patients with HCC, and may serve as a potential prognostic indicator for patients with multinodular HCC. Bioinformatics tools were utilized to predict the potential function of G9A, and the results indicated that G9A may modulate gene sets involved in RNA processing and DNA replication. G9A inhibition may suppress cell proliferation by arresting cells in G1 phase and increasing the expression level of microtubule-associated protein light chain 3β (MAP1LC3B) in Huh7 and HepG2 cells. In addition, an inverse association between the expression of G9A and LC3B was demonstrated in HCC tumor samples in the publically available GSE14520 dataset, which indicated that G9A may also have the potential to regulate MAP1LC3B expression in HCC tumor tissues. The results of the present study led to hypothesis that the G9A expression level may be of assistance in diagnosing HCC, and be a potential therapeutic target for HCC. The results provided novel evidence for additional understanding of the crucial role of G9A in tumorigenesis. D.A. Spandidos 2018-06 2018-04-25 /pmc/articles/PMC6004641/ /pubmed/29928350 http://dx.doi.org/10.3892/ol.2018.8572 Text en Copyright: © Qin 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
Qin, Jian
Li, Qingyun
Zeng, Zhi
Wu, Ping
Jiang, Yanping
Luo, Tao
Ji, Xiang
Zhang, Qiuping
Hao, Yarong
Chen, Lang
Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title_full Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title_fullStr Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title_full_unstemmed Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title_short Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
title_sort increased expression of g9a contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004641/
https://www.ncbi.nlm.nih.gov/pubmed/29928350
http://dx.doi.org/10.3892/ol.2018.8572
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