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NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status

N4-acetylcytidine (ac4C) is one type of RNA modification found in eukaryotes. RNA acetylation modifications are gradually expanding in oncology. However, the role of RNA acetylation modifications in colorectal cancer and its association with colorectal cancer microsatellite status remain unclear. Us...

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Detalles Bibliográficos
Autores principales: Zhang, Hailin, Shan, Wenqing, Yang, Zhenwei, Zhang, Yangyang, Wang, Meng, Gao, Liping, Zeng, Lingxiu, Zhao, Qiu, Liu, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026876/
https://www.ncbi.nlm.nih.gov/pubmed/36908042
http://dx.doi.org/10.1080/15592294.2023.2188667
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author Zhang, Hailin
Shan, Wenqing
Yang, Zhenwei
Zhang, Yangyang
Wang, Meng
Gao, Liping
Zeng, Lingxiu
Zhao, Qiu
Liu, Jing
author_facet Zhang, Hailin
Shan, Wenqing
Yang, Zhenwei
Zhang, Yangyang
Wang, Meng
Gao, Liping
Zeng, Lingxiu
Zhao, Qiu
Liu, Jing
author_sort Zhang, Hailin
collection PubMed
description N4-acetylcytidine (ac4C) is one type of RNA modification found in eukaryotes. RNA acetylation modifications are gradually expanding in oncology. However, the role of RNA acetylation modifications in colorectal cancer and its association with colorectal cancer microsatellite status remain unclear. Using public databases and in vitro experiments, we verified the expression and biological function of NAT10, as the key RNA acetylation modification enzyme, in colorectal cancer. The results showed that NAT10 was highly expressed in colorectal cancer, and significantly promoted colorectal cancer cell proliferation. NAT10 was also involved in several aspects of cell homoeostasis such as ion transport, calcium-dependent phospholipid binding, and RNA stability. NAT10 expression positively correlated with immune infiltration in colorectal cancer. We further constructed a risk regression model for mRNA acetylation in colorectal cancer using acetylation-related differential genes. We found that tumour immune infiltration, microsatellite instability (MSI) proportion, tumour immune mutation burden, and patient response to immunotherapy were positively correlated with risk scores. For the first time, our study showed that the level of mRNA acetylation modification level is elevated in colorectal cancer and positively correlates with immune infiltration and microsatellite status of patients. Based on our findings, NAT10 may be a new target for colorectal cancer treatment.
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spelling pubmed-100268762023-03-21 NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status Zhang, Hailin Shan, Wenqing Yang, Zhenwei Zhang, Yangyang Wang, Meng Gao, Liping Zeng, Lingxiu Zhao, Qiu Liu, Jing Epigenetics Research Paper N4-acetylcytidine (ac4C) is one type of RNA modification found in eukaryotes. RNA acetylation modifications are gradually expanding in oncology. However, the role of RNA acetylation modifications in colorectal cancer and its association with colorectal cancer microsatellite status remain unclear. Using public databases and in vitro experiments, we verified the expression and biological function of NAT10, as the key RNA acetylation modification enzyme, in colorectal cancer. The results showed that NAT10 was highly expressed in colorectal cancer, and significantly promoted colorectal cancer cell proliferation. NAT10 was also involved in several aspects of cell homoeostasis such as ion transport, calcium-dependent phospholipid binding, and RNA stability. NAT10 expression positively correlated with immune infiltration in colorectal cancer. We further constructed a risk regression model for mRNA acetylation in colorectal cancer using acetylation-related differential genes. We found that tumour immune infiltration, microsatellite instability (MSI) proportion, tumour immune mutation burden, and patient response to immunotherapy were positively correlated with risk scores. For the first time, our study showed that the level of mRNA acetylation modification level is elevated in colorectal cancer and positively correlates with immune infiltration and microsatellite status of patients. Based on our findings, NAT10 may be a new target for colorectal cancer treatment. Taylor & Francis 2023-03-12 /pmc/articles/PMC10026876/ /pubmed/36908042 http://dx.doi.org/10.1080/15592294.2023.2188667 Text en © 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Zhang, Hailin
Shan, Wenqing
Yang, Zhenwei
Zhang, Yangyang
Wang, Meng
Gao, Liping
Zeng, Lingxiu
Zhao, Qiu
Liu, Jing
NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title_full NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title_fullStr NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title_full_unstemmed NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title_short NAT10 mediated mRNA acetylation modification patterns associated with colon cancer progression and microsatellite status
title_sort nat10 mediated mrna acetylation modification patterns associated with colon cancer progression and microsatellite status
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10026876/
https://www.ncbi.nlm.nih.gov/pubmed/36908042
http://dx.doi.org/10.1080/15592294.2023.2188667
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