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Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) ranks fourth in cancer-related mortality worldwide. N1-methyladenosine (m1A), a methylation modification on RNA, is gaining attention for its role across diverse biological processes. However, m1A-related regulatory genes expression, its relationship with clinical prog...

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Autores principales: Shi, Qingmiao, Xue, Chen, Yuan, Xin, He, Yuting, Yu, Zujiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492257/
https://www.ncbi.nlm.nih.gov/pubmed/32934298
http://dx.doi.org/10.1038/s41598-020-72178-1
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author Shi, Qingmiao
Xue, Chen
Yuan, Xin
He, Yuting
Yu, Zujiang
author_facet Shi, Qingmiao
Xue, Chen
Yuan, Xin
He, Yuting
Yu, Zujiang
author_sort Shi, Qingmiao
collection PubMed
description Hepatocellular carcinoma (HCC) ranks fourth in cancer-related mortality worldwide. N1-methyladenosine (m1A), a methylation modification on RNA, is gaining attention for its role across diverse biological processes. However, m1A-related regulatory genes expression, its relationship with clinical prognosis, and its role in HCC remain unclear. In this study, we utilized The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) database to investigate alterations within 10 m1A-related regulatory genes and observed a high mutation frequency (23/363). Cox regression analysis and least absolute shrinkage and selection operator were used to explore the association between m1A-related regulatory genes expression and HCC patient survival and identified four regulators that were remarkably associated with HCC patient prognosis. Additionally, an independent cohort from International Cancer Genome Consortium was studied to validate our discoveries and found to be consistent with those in the TCGA dataset. In terms of mechanism, gene set enrichment analysis linked these four genes with various physiological roles in cell division, the MYC pathway, protein metabolism, and mitosis. Kyoto Encyclopedia of Genes and Genomes analysis revealed that PI3K/Akt signaling pathway had potential relevance to m1A-related regulatory genes in HCC. These findings indicate that m1A-related regulatory genes may play crucial roles in regulating HCC progression and be exploited for diagnostic and prognostic purposes.
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spelling pubmed-74922572020-09-16 Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma Shi, Qingmiao Xue, Chen Yuan, Xin He, Yuting Yu, Zujiang Sci Rep Article Hepatocellular carcinoma (HCC) ranks fourth in cancer-related mortality worldwide. N1-methyladenosine (m1A), a methylation modification on RNA, is gaining attention for its role across diverse biological processes. However, m1A-related regulatory genes expression, its relationship with clinical prognosis, and its role in HCC remain unclear. In this study, we utilized The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) database to investigate alterations within 10 m1A-related regulatory genes and observed a high mutation frequency (23/363). Cox regression analysis and least absolute shrinkage and selection operator were used to explore the association between m1A-related regulatory genes expression and HCC patient survival and identified four regulators that were remarkably associated with HCC patient prognosis. Additionally, an independent cohort from International Cancer Genome Consortium was studied to validate our discoveries and found to be consistent with those in the TCGA dataset. In terms of mechanism, gene set enrichment analysis linked these four genes with various physiological roles in cell division, the MYC pathway, protein metabolism, and mitosis. Kyoto Encyclopedia of Genes and Genomes analysis revealed that PI3K/Akt signaling pathway had potential relevance to m1A-related regulatory genes in HCC. These findings indicate that m1A-related regulatory genes may play crucial roles in regulating HCC progression and be exploited for diagnostic and prognostic purposes. Nature Publishing Group UK 2020-09-15 /pmc/articles/PMC7492257/ /pubmed/32934298 http://dx.doi.org/10.1038/s41598-020-72178-1 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Shi, Qingmiao
Xue, Chen
Yuan, Xin
He, Yuting
Yu, Zujiang
Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title_full Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title_fullStr Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title_full_unstemmed Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title_short Gene signatures and prognostic values of m1A-related regulatory genes in hepatocellular carcinoma
title_sort gene signatures and prognostic values of m1a-related regulatory genes in hepatocellular carcinoma
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492257/
https://www.ncbi.nlm.nih.gov/pubmed/32934298
http://dx.doi.org/10.1038/s41598-020-72178-1
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