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Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers

BACKGROUND: As one of the most abundant post‐transcriptional mRNA modifications, N6‐methyladenosine (m6A) has attracted extensive attention from scientists. Emerging evidence indicates that m6A modification plays a significant role in cancer‐related signalling pathways. Existing research demonstrate...

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Autores principales: Feng, Huiru, Yuan, Xiaofei, Wu, Shuting, Yuan, Yue, Cui, Linchong, Lin, Danfan, Peng, Xiaohong, Liu, Xiong, Wang, Fan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9816932/
https://www.ncbi.nlm.nih.gov/pubmed/36162823
http://dx.doi.org/10.1111/cpr.13340
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author Feng, Huiru
Yuan, Xiaofei
Wu, Shuting
Yuan, Yue
Cui, Linchong
Lin, Danfan
Peng, Xiaohong
Liu, Xiong
Wang, Fan
author_facet Feng, Huiru
Yuan, Xiaofei
Wu, Shuting
Yuan, Yue
Cui, Linchong
Lin, Danfan
Peng, Xiaohong
Liu, Xiong
Wang, Fan
author_sort Feng, Huiru
collection PubMed
description BACKGROUND: As one of the most abundant post‐transcriptional mRNA modifications, N6‐methyladenosine (m6A) has attracted extensive attention from scientists. Emerging evidence indicates that m6A modification plays a significant role in cancer‐related signalling pathways. Existing research demonstrates that m6A modifications were also identified in miRNAs and contribute to cancer‐related signalling pathways. METHODS: A literature retrieval has been performed to collect m6A‐miRNA‐related original articles published in recent years. Later, a systematic analysis has been conducted to abstract and classify the relationships between m6A modification and miRNAs, and their contributions to tumorigenesis and cancer development. RESULTS: Accumulating literature provides important insights into multiple relationships between m6A modifications and miRNAs. Mechanically, m6A writer and eraser alter pri‐miRNAs m6A levels, and m6A readers could dually modulate pri‐miRNAs processing and pri‐miRNAs degradation. It is also been demonstrated that miRNAs impair m6A regulators' translation to influence m6A medication function in return. Aberrant expressions of m6A regulators and miRNAs could dysregulate proliferative, apoptosis, cell adhesion‐related, and malignant transformation signalling pathways, and contribute to tumour occurrence and development. CONCLUSION: This review summarizes the interrelationship between m6A modification and miRNAs; highlights the combined effects of each type of m6A regulator and miRNAs in cancers. These findings enhance our understanding of m6A‐miRNAs' multiple interactions and significant modulatory role in tumorigenesis and progression.
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spelling pubmed-98169322023-01-06 Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers Feng, Huiru Yuan, Xiaofei Wu, Shuting Yuan, Yue Cui, Linchong Lin, Danfan Peng, Xiaohong Liu, Xiong Wang, Fan Cell Prolif Reviews BACKGROUND: As one of the most abundant post‐transcriptional mRNA modifications, N6‐methyladenosine (m6A) has attracted extensive attention from scientists. Emerging evidence indicates that m6A modification plays a significant role in cancer‐related signalling pathways. Existing research demonstrates that m6A modifications were also identified in miRNAs and contribute to cancer‐related signalling pathways. METHODS: A literature retrieval has been performed to collect m6A‐miRNA‐related original articles published in recent years. Later, a systematic analysis has been conducted to abstract and classify the relationships between m6A modification and miRNAs, and their contributions to tumorigenesis and cancer development. RESULTS: Accumulating literature provides important insights into multiple relationships between m6A modifications and miRNAs. Mechanically, m6A writer and eraser alter pri‐miRNAs m6A levels, and m6A readers could dually modulate pri‐miRNAs processing and pri‐miRNAs degradation. It is also been demonstrated that miRNAs impair m6A regulators' translation to influence m6A medication function in return. Aberrant expressions of m6A regulators and miRNAs could dysregulate proliferative, apoptosis, cell adhesion‐related, and malignant transformation signalling pathways, and contribute to tumour occurrence and development. CONCLUSION: This review summarizes the interrelationship between m6A modification and miRNAs; highlights the combined effects of each type of m6A regulator and miRNAs in cancers. These findings enhance our understanding of m6A‐miRNAs' multiple interactions and significant modulatory role in tumorigenesis and progression. John Wiley and Sons Inc. 2022-09-26 /pmc/articles/PMC9816932/ /pubmed/36162823 http://dx.doi.org/10.1111/cpr.13340 Text en © 2022 The Authors. Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Feng, Huiru
Yuan, Xiaofei
Wu, Shuting
Yuan, Yue
Cui, Linchong
Lin, Danfan
Peng, Xiaohong
Liu, Xiong
Wang, Fan
Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title_full Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title_fullStr Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title_full_unstemmed Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title_short Effects of writers, erasers and readers within miRNA‐related m6A modification in cancers
title_sort effects of writers, erasers and readers within mirna‐related m6a modification in cancers
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9816932/
https://www.ncbi.nlm.nih.gov/pubmed/36162823
http://dx.doi.org/10.1111/cpr.13340
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