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Insights into the regulatory role of RNA methylation modifications in glioma
Epitranscriptomic abnormalities, which are highly prevalent in primary central nervous system malignancies, have been identified as crucial contributors to the development and progression of gliomas. RNA epitranscriptomic modifications, particularly the reversible modification methylation, have been...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644640/ https://www.ncbi.nlm.nih.gov/pubmed/37964279 http://dx.doi.org/10.1186/s12967-023-04653-y |
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author | Long, Shengrong Yan, Yu Xu, Hongyu Wang, Lesheng Jiang, Jiazhi Xu, Ziyue Liu, Runming Zhou, Qiangqiang Huang, Xiaopeng Chen, Jincao Li, Zhiqiang Wei, Wei Li, Xiang |
author_facet | Long, Shengrong Yan, Yu Xu, Hongyu Wang, Lesheng Jiang, Jiazhi Xu, Ziyue Liu, Runming Zhou, Qiangqiang Huang, Xiaopeng Chen, Jincao Li, Zhiqiang Wei, Wei Li, Xiang |
author_sort | Long, Shengrong |
collection | PubMed |
description | Epitranscriptomic abnormalities, which are highly prevalent in primary central nervous system malignancies, have been identified as crucial contributors to the development and progression of gliomas. RNA epitranscriptomic modifications, particularly the reversible modification methylation, have been observed throughout the RNA cycle. Epitranscriptomic modifications, which regulate RNA transcription and translation, have profound biological implications. These modifications are associated with the development of several cancer types. Notably, three main protein types—writers, erasers, and readers, in conjunction with other related proteins, mediate these epitranscriptomic changes. This review primarily focuses on the role of recently identified RNA methylation modifications in gliomas, such as N6-methyladenosine (m6A), 5-methylcytosine (m5C), N7-methylguanosine (m7G), and N1-methyladenosine (m1A). We delved into their corresponding writers, erasers, readers, and related binding proteins to propose new approaches and prognostic indicators for patients with glioma. |
format | Online Article Text |
id | pubmed-10644640 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-106446402023-11-14 Insights into the regulatory role of RNA methylation modifications in glioma Long, Shengrong Yan, Yu Xu, Hongyu Wang, Lesheng Jiang, Jiazhi Xu, Ziyue Liu, Runming Zhou, Qiangqiang Huang, Xiaopeng Chen, Jincao Li, Zhiqiang Wei, Wei Li, Xiang J Transl Med Review Epitranscriptomic abnormalities, which are highly prevalent in primary central nervous system malignancies, have been identified as crucial contributors to the development and progression of gliomas. RNA epitranscriptomic modifications, particularly the reversible modification methylation, have been observed throughout the RNA cycle. Epitranscriptomic modifications, which regulate RNA transcription and translation, have profound biological implications. These modifications are associated with the development of several cancer types. Notably, three main protein types—writers, erasers, and readers, in conjunction with other related proteins, mediate these epitranscriptomic changes. This review primarily focuses on the role of recently identified RNA methylation modifications in gliomas, such as N6-methyladenosine (m6A), 5-methylcytosine (m5C), N7-methylguanosine (m7G), and N1-methyladenosine (m1A). We delved into their corresponding writers, erasers, readers, and related binding proteins to propose new approaches and prognostic indicators for patients with glioma. BioMed Central 2023-11-14 /pmc/articles/PMC10644640/ /pubmed/37964279 http://dx.doi.org/10.1186/s12967-023-04653-y Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Long, Shengrong Yan, Yu Xu, Hongyu Wang, Lesheng Jiang, Jiazhi Xu, Ziyue Liu, Runming Zhou, Qiangqiang Huang, Xiaopeng Chen, Jincao Li, Zhiqiang Wei, Wei Li, Xiang Insights into the regulatory role of RNA methylation modifications in glioma |
title | Insights into the regulatory role of RNA methylation modifications in glioma |
title_full | Insights into the regulatory role of RNA methylation modifications in glioma |
title_fullStr | Insights into the regulatory role of RNA methylation modifications in glioma |
title_full_unstemmed | Insights into the regulatory role of RNA methylation modifications in glioma |
title_short | Insights into the regulatory role of RNA methylation modifications in glioma |
title_sort | insights into the regulatory role of rna methylation modifications in glioma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644640/ https://www.ncbi.nlm.nih.gov/pubmed/37964279 http://dx.doi.org/10.1186/s12967-023-04653-y |
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