Cargando…
N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies
The N6-methyladenosine (m6A) modification is a dynamic and reversible epigenetic modification, which is co-transcriptionally deposited by a methyltransferase complex, removed by a demethylase, and recognized by reader proteins. Mechanistically, m6A modification regulates the expression levels of mRN...
Autores principales: | , , , , , , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8082653/ https://www.ncbi.nlm.nih.gov/pubmed/33926508 http://dx.doi.org/10.1186/s13046-021-01952-4 |
_version_ | 1783685882983743488 |
---|---|
author | Tan, Fenghua Zhao, Mengyao Xiong, Fang Wang, Yumin Zhang, Shanshan Gong, Zhaojian Li, Xiayu He, Yi Shi, Lei Wang, Fuyan Xiang, Bo Zhou, Ming Li, Xiaoling Li, Yong Li, Guiyuan Zeng, Zhaoyang Xiong, Wei Guo, Can |
author_facet | Tan, Fenghua Zhao, Mengyao Xiong, Fang Wang, Yumin Zhang, Shanshan Gong, Zhaojian Li, Xiayu He, Yi Shi, Lei Wang, Fuyan Xiang, Bo Zhou, Ming Li, Xiaoling Li, Yong Li, Guiyuan Zeng, Zhaoyang Xiong, Wei Guo, Can |
author_sort | Tan, Fenghua |
collection | PubMed |
description | The N6-methyladenosine (m6A) modification is a dynamic and reversible epigenetic modification, which is co-transcriptionally deposited by a methyltransferase complex, removed by a demethylase, and recognized by reader proteins. Mechanistically, m6A modification regulates the expression levels of mRNA and nocoding RNA by modulating the fate of modified RNA molecules, such as RNA splicing, nuclear transport, translation, and stability. Several studies have shown that m6A modification is dysregulated in the progression of multiple diseases, especially human tumors. We emphasized that the dysregulation of m6A modification affects different signal transduction pathways and involves in the biological processes underlying tumor cell proliferation, apoptosis, invasion and migration, and metabolic reprogramming, and discuss the effects on different cancer treatment. |
format | Online Article Text |
id | pubmed-8082653 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-80826532021-04-29 N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies Tan, Fenghua Zhao, Mengyao Xiong, Fang Wang, Yumin Zhang, Shanshan Gong, Zhaojian Li, Xiayu He, Yi Shi, Lei Wang, Fuyan Xiang, Bo Zhou, Ming Li, Xiaoling Li, Yong Li, Guiyuan Zeng, Zhaoyang Xiong, Wei Guo, Can J Exp Clin Cancer Res Review The N6-methyladenosine (m6A) modification is a dynamic and reversible epigenetic modification, which is co-transcriptionally deposited by a methyltransferase complex, removed by a demethylase, and recognized by reader proteins. Mechanistically, m6A modification regulates the expression levels of mRNA and nocoding RNA by modulating the fate of modified RNA molecules, such as RNA splicing, nuclear transport, translation, and stability. Several studies have shown that m6A modification is dysregulated in the progression of multiple diseases, especially human tumors. We emphasized that the dysregulation of m6A modification affects different signal transduction pathways and involves in the biological processes underlying tumor cell proliferation, apoptosis, invasion and migration, and metabolic reprogramming, and discuss the effects on different cancer treatment. BioMed Central 2021-04-29 /pmc/articles/PMC8082653/ /pubmed/33926508 http://dx.doi.org/10.1186/s13046-021-01952-4 Text en © The Author(s) 2021 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 Tan, Fenghua Zhao, Mengyao Xiong, Fang Wang, Yumin Zhang, Shanshan Gong, Zhaojian Li, Xiayu He, Yi Shi, Lei Wang, Fuyan Xiang, Bo Zhou, Ming Li, Xiaoling Li, Yong Li, Guiyuan Zeng, Zhaoyang Xiong, Wei Guo, Can N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title | N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title_full | N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title_fullStr | N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title_full_unstemmed | N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title_short | N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
title_sort | n6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8082653/ https://www.ncbi.nlm.nih.gov/pubmed/33926508 http://dx.doi.org/10.1186/s13046-021-01952-4 |
work_keys_str_mv | AT tanfenghua n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT zhaomengyao n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT xiongfang n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT wangyumin n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT zhangshanshan n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT gongzhaojian n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT lixiayu n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT heyi n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT shilei n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT wangfuyan n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT xiangbo n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT zhouming n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT lixiaoling n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT liyong n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT liguiyuan n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT zengzhaoyang n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT xiongwei n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies AT guocan n6methyladenosinedependentsignallingincancerprogressionandinsightsintocancertherapies |