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Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model

Keloids are formed due to abnormal hyperplasia of the skin connective tissue. We explored the relationship between N6‐methyladenosine (m6A)‐related genes and keloids. The transcriptomic datasets (GSE44270 and GSE185309) of keloid and normal skin tissues samples were obtained from the Gene Expression...

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Autores principales: Yang, Ronghua, Wang, Xiaoxiang, Zheng, Wenlian, Chen, Wentao, Gan, Wenjun, Qin, Xinchi, Huang, Jie, Chen, Xiaodong, Zhou, Sitong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10410345/
https://www.ncbi.nlm.nih.gov/pubmed/36896881
http://dx.doi.org/10.1111/iwj.14144
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author Yang, Ronghua
Wang, Xiaoxiang
Zheng, Wenlian
Chen, Wentao
Gan, Wenjun
Qin, Xinchi
Huang, Jie
Chen, Xiaodong
Zhou, Sitong
author_facet Yang, Ronghua
Wang, Xiaoxiang
Zheng, Wenlian
Chen, Wentao
Gan, Wenjun
Qin, Xinchi
Huang, Jie
Chen, Xiaodong
Zhou, Sitong
author_sort Yang, Ronghua
collection PubMed
description Keloids are formed due to abnormal hyperplasia of the skin connective tissue. We explored the relationship between N6‐methyladenosine (m6A)‐related genes and keloids. The transcriptomic datasets (GSE44270 and GSE185309) of keloid and normal skin tissues samples were obtained from the Gene Expression Omnibus database. We constructed the m6A landscape and verified the corresponding genes using immunohistochemistry. We extracted hub genes for unsupervised clustering analysis using protein–protein interaction (PPI) network; gene ontology enrichment analysis was performed to determine the biological processes or functions affected by the differentially expressed genes (DEGs). We performed immune infiltration analysis to determine the relationship between keloids and the immune microenvironment using single‐sample gene set enrichment analysis and CIBERSORT. Differential expression of several m6A genes was observed between the two groups; insulin‐like growth factor 2 mRNA‐binding protein 3 (IGF2BP3) was significantly upregulated in keloid patients. PPI analysis elucidated six genes with significant differences between the two keloid sample groups. Enrichment analysis revealed that the DEGs were mainly enriched in cell division, proliferation, and metabolism. Moreover, significant differences in immunity‐related pathways were observed. Therefore, the results of this study will provide a reference for the elucidation of the pathogenesis and therapeutic targets of keloids.
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spelling pubmed-104103452023-08-10 Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model Yang, Ronghua Wang, Xiaoxiang Zheng, Wenlian Chen, Wentao Gan, Wenjun Qin, Xinchi Huang, Jie Chen, Xiaodong Zhou, Sitong Int Wound J Original Articles Keloids are formed due to abnormal hyperplasia of the skin connective tissue. We explored the relationship between N6‐methyladenosine (m6A)‐related genes and keloids. The transcriptomic datasets (GSE44270 and GSE185309) of keloid and normal skin tissues samples were obtained from the Gene Expression Omnibus database. We constructed the m6A landscape and verified the corresponding genes using immunohistochemistry. We extracted hub genes for unsupervised clustering analysis using protein–protein interaction (PPI) network; gene ontology enrichment analysis was performed to determine the biological processes or functions affected by the differentially expressed genes (DEGs). We performed immune infiltration analysis to determine the relationship between keloids and the immune microenvironment using single‐sample gene set enrichment analysis and CIBERSORT. Differential expression of several m6A genes was observed between the two groups; insulin‐like growth factor 2 mRNA‐binding protein 3 (IGF2BP3) was significantly upregulated in keloid patients. PPI analysis elucidated six genes with significant differences between the two keloid sample groups. Enrichment analysis revealed that the DEGs were mainly enriched in cell division, proliferation, and metabolism. Moreover, significant differences in immunity‐related pathways were observed. Therefore, the results of this study will provide a reference for the elucidation of the pathogenesis and therapeutic targets of keloids. Blackwell Publishing Ltd 2023-03-10 /pmc/articles/PMC10410345/ /pubmed/36896881 http://dx.doi.org/10.1111/iwj.14144 Text en © 2023 The Authors. International Wound Journal published by Medicalhelplines.com Inc and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Yang, Ronghua
Wang, Xiaoxiang
Zheng, Wenlian
Chen, Wentao
Gan, Wenjun
Qin, Xinchi
Huang, Jie
Chen, Xiaodong
Zhou, Sitong
Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title_full Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title_fullStr Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title_full_unstemmed Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title_short Bioinformatics analysis and verification of m6A related genes based on the construction of keloid diagnostic model
title_sort bioinformatics analysis and verification of m6a related genes based on the construction of keloid diagnostic model
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10410345/
https://www.ncbi.nlm.nih.gov/pubmed/36896881
http://dx.doi.org/10.1111/iwj.14144
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