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Epigenetic Regulation of m(6)A Modifications in Human Cancer
N6-methyladenosine (m(6)A) is the most prevalent internal RNA modification, especially within eukaryotic messenger RNAs (mRNAs). m(6)A modifications of RNA regulate splicing, translocation, stability, and translation into proteins. m(6)A modifications are catalyzed by RNA methyltransferases, such as...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Gene & Cell Therapy
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938965/ https://www.ncbi.nlm.nih.gov/pubmed/31887551 http://dx.doi.org/10.1016/j.omtn.2019.11.022 |
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author | Zhao, Wei Qi, Xiaoqian Liu, Lina Liu, Zihao Ma, Shiqing Wu, Jie |
author_facet | Zhao, Wei Qi, Xiaoqian Liu, Lina Liu, Zihao Ma, Shiqing Wu, Jie |
author_sort | Zhao, Wei |
collection | PubMed |
description | N6-methyladenosine (m(6)A) is the most prevalent internal RNA modification, especially within eukaryotic messenger RNAs (mRNAs). m(6)A modifications of RNA regulate splicing, translocation, stability, and translation into proteins. m(6)A modifications are catalyzed by RNA methyltransferases, such as METTL3, METTL14, and WTAP (writers); the modifications are removed by the demethylases fat mass and obesity-associated protein (FTO) and ALKBH5 (ALKB homolog 5) (erasers); and the modifications are recognized by m(6)A-binding proteins, such as YTHDF domain-containing proteins and IGF2BPs (readers). Abnormal changes in the m(6)A levels of these genes are closely related to tumor occurrence and development. In this paper, we review the role of m(6)A in human cancer and summarize its prospective applications in cancer. |
format | Online Article Text |
id | pubmed-6938965 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | American Society of Gene & Cell Therapy |
record_format | MEDLINE/PubMed |
spelling | pubmed-69389652020-01-06 Epigenetic Regulation of m(6)A Modifications in Human Cancer Zhao, Wei Qi, Xiaoqian Liu, Lina Liu, Zihao Ma, Shiqing Wu, Jie Mol Ther Nucleic Acids Article N6-methyladenosine (m(6)A) is the most prevalent internal RNA modification, especially within eukaryotic messenger RNAs (mRNAs). m(6)A modifications of RNA regulate splicing, translocation, stability, and translation into proteins. m(6)A modifications are catalyzed by RNA methyltransferases, such as METTL3, METTL14, and WTAP (writers); the modifications are removed by the demethylases fat mass and obesity-associated protein (FTO) and ALKBH5 (ALKB homolog 5) (erasers); and the modifications are recognized by m(6)A-binding proteins, such as YTHDF domain-containing proteins and IGF2BPs (readers). Abnormal changes in the m(6)A levels of these genes are closely related to tumor occurrence and development. In this paper, we review the role of m(6)A in human cancer and summarize its prospective applications in cancer. American Society of Gene & Cell Therapy 2019-11-29 /pmc/articles/PMC6938965/ /pubmed/31887551 http://dx.doi.org/10.1016/j.omtn.2019.11.022 Text en © 2019 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Zhao, Wei Qi, Xiaoqian Liu, Lina Liu, Zihao Ma, Shiqing Wu, Jie Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title | Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title_full | Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title_fullStr | Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title_full_unstemmed | Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title_short | Epigenetic Regulation of m(6)A Modifications in Human Cancer |
title_sort | epigenetic regulation of m(6)a modifications in human cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6938965/ https://www.ncbi.nlm.nih.gov/pubmed/31887551 http://dx.doi.org/10.1016/j.omtn.2019.11.022 |
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