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Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease characterized by incomplete reversible airway obstruction, with high mortality and disability rates, and smoking is the primary risk factor for COPD. Studies performed to date have confirmed that iron and ferro...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9011264/ https://www.ncbi.nlm.nih.gov/pubmed/35433978 http://dx.doi.org/10.21037/atm-22-1009 |
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author | Lin, Zhiwei Xu, Yifan Guan, Lili Qin, Lijie Ding, Jiabin Zhang, Qingling Zhou, Luqian |
author_facet | Lin, Zhiwei Xu, Yifan Guan, Lili Qin, Lijie Ding, Jiabin Zhang, Qingling Zhou, Luqian |
author_sort | Lin, Zhiwei |
collection | PubMed |
description | BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease characterized by incomplete reversible airway obstruction, with high mortality and disability rates, and smoking is the primary risk factor for COPD. Studies performed to date have confirmed that iron and ferroptosis play crucial roles in the development of cigarette smoke-induced COPD, but the exact mechanisms have not been fully elucidated. METHODS: The microarray datasets GSE10006, GSE11784, and GSE20257 were downloaded from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs) between COPD smokers and non-smokers airway epithelial. Protein-protein interaction (PPI) and hub gene networks were constructed using the STRING database and Cytoscape software. At the same time, the 3 datasets were screened for ferroptosis-related genes that were co-differentially expressed. The ferroptosis-related hub genes (FRHGs) that overlapped with the ferroptosis-related genes and hub genes were then identified. Next, the mRNA-miRNA network was constructed, and Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for target genes were performed. Finally, GSE19407, GSE994, and GSE27973 were used to evaluate the expression of hub genes. RESULTS: We identified 7 potential FRHGs (NQO1, AKR1C3, AKR1C1, GPX2, TXNRD1, SRXN1, SLC7A11), which showed good diagnostic properties. The molecular functions (MFs) of FRHGs mainly influence biological processes (BPs) responding to oxidative stress. Nrf2 pathways may be the key pathways regulating ferroptosis in cigarette smoke-induced COPD. Meanwhile, co-expressed mRNAs and miRNAs were selected to construct mRNA-miRNA interaction networks. Furthermore, based on the 7 FRHGs mentioned above, we found that benzoic acid showed high drug targeting relevance. CONCLUSIONS: This work identified 7 FRHGs as potential biomarkers for the diagnosis and treatment of COPD and provided insights into the mechanisms of disease development in cigarette smoke-induced COPD at the transcriptome level. |
format | Online Article Text |
id | pubmed-9011264 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-90112642022-04-16 Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease Lin, Zhiwei Xu, Yifan Guan, Lili Qin, Lijie Ding, Jiabin Zhang, Qingling Zhou, Luqian Ann Transl Med Original Article BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease characterized by incomplete reversible airway obstruction, with high mortality and disability rates, and smoking is the primary risk factor for COPD. Studies performed to date have confirmed that iron and ferroptosis play crucial roles in the development of cigarette smoke-induced COPD, but the exact mechanisms have not been fully elucidated. METHODS: The microarray datasets GSE10006, GSE11784, and GSE20257 were downloaded from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes (DEGs) between COPD smokers and non-smokers airway epithelial. Protein-protein interaction (PPI) and hub gene networks were constructed using the STRING database and Cytoscape software. At the same time, the 3 datasets were screened for ferroptosis-related genes that were co-differentially expressed. The ferroptosis-related hub genes (FRHGs) that overlapped with the ferroptosis-related genes and hub genes were then identified. Next, the mRNA-miRNA network was constructed, and Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for target genes were performed. Finally, GSE19407, GSE994, and GSE27973 were used to evaluate the expression of hub genes. RESULTS: We identified 7 potential FRHGs (NQO1, AKR1C3, AKR1C1, GPX2, TXNRD1, SRXN1, SLC7A11), which showed good diagnostic properties. The molecular functions (MFs) of FRHGs mainly influence biological processes (BPs) responding to oxidative stress. Nrf2 pathways may be the key pathways regulating ferroptosis in cigarette smoke-induced COPD. Meanwhile, co-expressed mRNAs and miRNAs were selected to construct mRNA-miRNA interaction networks. Furthermore, based on the 7 FRHGs mentioned above, we found that benzoic acid showed high drug targeting relevance. CONCLUSIONS: This work identified 7 FRHGs as potential biomarkers for the diagnosis and treatment of COPD and provided insights into the mechanisms of disease development in cigarette smoke-induced COPD at the transcriptome level. AME Publishing Company 2022-03 /pmc/articles/PMC9011264/ /pubmed/35433978 http://dx.doi.org/10.21037/atm-22-1009 Text en 2022 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) . |
spellingShingle | Original Article Lin, Zhiwei Xu, Yifan Guan, Lili Qin, Lijie Ding, Jiabin Zhang, Qingling Zhou, Luqian Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title | Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title_full | Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title_fullStr | Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title_full_unstemmed | Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title_short | Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
title_sort | seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9011264/ https://www.ncbi.nlm.nih.gov/pubmed/35433978 http://dx.doi.org/10.21037/atm-22-1009 |
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