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Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease

This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson's disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the d...

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Autores principales: Quan, Wei, Li, Jia, Liu, Li, Zhang, Qinghui, Qin, Yidan, Pei, Xiaochen, Chen, Jiajun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712163/
https://www.ncbi.nlm.nih.gov/pubmed/34966539
http://dx.doi.org/10.1155/2021/9919129
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author Quan, Wei
Li, Jia
Liu, Li
Zhang, Qinghui
Qin, Yidan
Pei, Xiaochen
Chen, Jiajun
author_facet Quan, Wei
Li, Jia
Liu, Li
Zhang, Qinghui
Qin, Yidan
Pei, Xiaochen
Chen, Jiajun
author_sort Quan, Wei
collection PubMed
description This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson's disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differentially expressed genes and function enrichment analysis of the two sets of data and found that the expression of the m6A-modification gene HNRNPC was significantly downregulated in the PD group, and it played an important role in DNA metabolism, RNA metabolism, and RNA processing and may be involved in PD. Then, we constructed the HNRNPC differential expression cell line to study the role of this gene in the pathogenesis of PD. The results showed that overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors IFN-β, IL-6, and TNF-α, suggesting that HNRNPC may cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation. Our study also has certain limitations. For example, the data of the experimental group and the validation group come from different cell types, and the data of the experimental group involve individuals with G2019S LRRK2 mutations. In addition, due to the low expression of HNRNPC in PC12 cells, we used the method of overexpressing this gene to study its function. All these factors may cause our conclusions to be biased. Therefore, more research is still needed to corroborate it in the future.
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spelling pubmed-87121632021-12-28 Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease Quan, Wei Li, Jia Liu, Li Zhang, Qinghui Qin, Yidan Pei, Xiaochen Chen, Jiajun Parkinsons Dis Research Article This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson's disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differentially expressed genes and function enrichment analysis of the two sets of data and found that the expression of the m6A-modification gene HNRNPC was significantly downregulated in the PD group, and it played an important role in DNA metabolism, RNA metabolism, and RNA processing and may be involved in PD. Then, we constructed the HNRNPC differential expression cell line to study the role of this gene in the pathogenesis of PD. The results showed that overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors IFN-β, IL-6, and TNF-α, suggesting that HNRNPC may cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation. Our study also has certain limitations. For example, the data of the experimental group and the validation group come from different cell types, and the data of the experimental group involve individuals with G2019S LRRK2 mutations. In addition, due to the low expression of HNRNPC in PC12 cells, we used the method of overexpressing this gene to study its function. All these factors may cause our conclusions to be biased. Therefore, more research is still needed to corroborate it in the future. Hindawi 2021-12-20 /pmc/articles/PMC8712163/ /pubmed/34966539 http://dx.doi.org/10.1155/2021/9919129 Text en Copyright © 2021 Wei Quan et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Quan, Wei
Li, Jia
Liu, Li
Zhang, Qinghui
Qin, Yidan
Pei, Xiaochen
Chen, Jiajun
Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title_full Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title_fullStr Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title_full_unstemmed Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title_short Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson's Disease
title_sort influence of n6-methyladenosine modification gene hnrnpc on cell phenotype in parkinson's disease
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712163/
https://www.ncbi.nlm.nih.gov/pubmed/34966539
http://dx.doi.org/10.1155/2021/9919129
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