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m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion
N6-methyladenosine (m(6)A) methylation is the most universal internal modification in eukaryotic mRNA. With elaborate functions executed by m(6)A writers, erasers, and readers, m(6)A modulation is involved in myriad physiological and pathological processes. Extensive studies have demonstrated m(6)A...
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/PMC9976403/ https://www.ncbi.nlm.nih.gov/pubmed/36859310 http://dx.doi.org/10.1186/s12943-022-01704-8 |
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author | Cao, Xiaoxue Geng, Qishun Fan, Danping Wang, Qiong Wang, Xing Zhang, Mengxiao Zhao, Lu Jiao, Yi Deng, Tingting Liu, Honglin Zhou, Jing Jia, Liqun Xiao, Cheng |
author_facet | Cao, Xiaoxue Geng, Qishun Fan, Danping Wang, Qiong Wang, Xing Zhang, Mengxiao Zhao, Lu Jiao, Yi Deng, Tingting Liu, Honglin Zhou, Jing Jia, Liqun Xiao, Cheng |
author_sort | Cao, Xiaoxue |
collection | PubMed |
description | N6-methyladenosine (m(6)A) methylation is the most universal internal modification in eukaryotic mRNA. With elaborate functions executed by m(6)A writers, erasers, and readers, m(6)A modulation is involved in myriad physiological and pathological processes. Extensive studies have demonstrated m(6)A modulation in diverse tumours, with effects on tumorigenesis, metastasis, and resistance. Recent evidence has revealed an emerging role of m(6)A modulation in tumour immunoregulation, and divergent m(6)A methylation patterns have been revealed in the tumour microenvironment. To depict the regulatory role of m(6)A methylation in the tumour immune microenvironment (TIME) and its effect on immune evasion, this review focuses on the TIME, which is characterized by hypoxia, metabolic reprogramming, acidity, and immunosuppression, and outlines the m(6)A-regulated TIME and immune evasion under divergent stimuli. Furthermore, m(6)A modulation patterns in anti-tumour immune cells are summarized. |
format | Online Article Text |
id | pubmed-9976403 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-99764032023-03-02 m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion Cao, Xiaoxue Geng, Qishun Fan, Danping Wang, Qiong Wang, Xing Zhang, Mengxiao Zhao, Lu Jiao, Yi Deng, Tingting Liu, Honglin Zhou, Jing Jia, Liqun Xiao, Cheng Mol Cancer Review N6-methyladenosine (m(6)A) methylation is the most universal internal modification in eukaryotic mRNA. With elaborate functions executed by m(6)A writers, erasers, and readers, m(6)A modulation is involved in myriad physiological and pathological processes. Extensive studies have demonstrated m(6)A modulation in diverse tumours, with effects on tumorigenesis, metastasis, and resistance. Recent evidence has revealed an emerging role of m(6)A modulation in tumour immunoregulation, and divergent m(6)A methylation patterns have been revealed in the tumour microenvironment. To depict the regulatory role of m(6)A methylation in the tumour immune microenvironment (TIME) and its effect on immune evasion, this review focuses on the TIME, which is characterized by hypoxia, metabolic reprogramming, acidity, and immunosuppression, and outlines the m(6)A-regulated TIME and immune evasion under divergent stimuli. Furthermore, m(6)A modulation patterns in anti-tumour immune cells are summarized. BioMed Central 2023-03-01 /pmc/articles/PMC9976403/ /pubmed/36859310 http://dx.doi.org/10.1186/s12943-022-01704-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 Cao, Xiaoxue Geng, Qishun Fan, Danping Wang, Qiong Wang, Xing Zhang, Mengxiao Zhao, Lu Jiao, Yi Deng, Tingting Liu, Honglin Zhou, Jing Jia, Liqun Xiao, Cheng m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title | m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title_full | m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title_fullStr | m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title_full_unstemmed | m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title_short | m(6)A methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
title_sort | m(6)a methylation: a process reshaping the tumour immune microenvironment and regulating immune evasion |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9976403/ https://www.ncbi.nlm.nih.gov/pubmed/36859310 http://dx.doi.org/10.1186/s12943-022-01704-8 |
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