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CXCL10、SCGN和H2BC5作为受丙型肝炎病毒感染调控的潜在关键基因。

CXCL10, SCGN, and H2BC5 as Potential Key Genes Regulated by HCV Infection.

作者信息

Yıldırım Çiğdem, Yay Fatih, İmre Ayfer, Soysal Orçun, Yıldırım Hasan Çağrı

机构信息

Department of Infectious Diseases and Clinical Microbiology, Nigde Training and Research Hospital, 51100 Nigde, Turkey.

Clinical Biochemistry Laboratory, Nigde Training and Research Hospital, 51100 Nigde, Turkey.

出版信息

Genes (Basel). 2024 Nov 22;15(12):1502. doi: 10.3390/genes15121502.

DOI:10.3390/genes15121502
PMID:39766770
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11675613/
Abstract

Hepatitis C infections are the main causes of fatal clinical conditions such as cirrhosis and HCC development, and biomarkers are needed to predict the development of these complications. Therefore, it is important to first determine which genes are deregulated in HCV-cells compared to healthy individuals. In our study, we aimed to identify the genes that are commonly upregulated or downregulated in HCV-infected cells using two different databases. In this study, differentially expressed genes (DEGs) that were commonly upregulated or downregulated were identified using publicly available databases GSE66842 and GSE84587. Afterwards, the interactions of DEG products with each other and other proteins were examined using the STRING database. Enrichment analyses of DEGs were performed using the Enrichr-KG web tool including the Gene Ontology Biological Process, KEGG, Jensen_DISEASES and DisGeNET libraries. miRNAs targeting DEGs were detected using miRDB and TargetScanHuman8.0. In HCV-infected cells, the expression is increased in both databases, while the and () expression is decreased. No direct interaction was found among CXCL10, SCGN, H2BC5 in the top ten proteins. CXCL10 is a member of Hepatitis C and viral protein interactions with cytokine and cytokine receptor KEGG pathways. H2BC5 is a member of viral carcinogenesis KEGG pathways. Predicted overlapping miRNAs targeted by common DEGs were as follows: 59 were where was the estimated target, 22 where was the estimated target and where () was the estimated target. Our study identified genes that were upregulated or downregulated in HCV-infected cells in both databases and miRNAs associated with these genes, using two different databases. This study creates groundwork for future studies to investigate whether these genes can predict HCV prognosis and HCV-associated HCC development.

摘要

丙型肝炎感染是导致肝硬化和肝癌发展等致命临床病症的主要原因,因此需要生物标志物来预测这些并发症的发生。所以,首先确定与健康个体相比,丙型肝炎病毒(HCV)感染细胞中哪些基因表达失调至关重要。在我们的研究中,我们旨在使用两个不同的数据库来鉴定HCV感染细胞中普遍上调或下调的基因。在本研究中,利用公开可用的数据库GSE66842和GSE84587鉴定了普遍上调或下调的差异表达基因(DEG)。之后,使用STRING数据库检查DEG产物之间以及与其他蛋白质的相互作用。使用Enrichr-KG网络工具对DEG进行富集分析,该工具包括基因本体生物学过程、KEGG、Jensen_DISEASES和DisGeNET库。使用miRDB和TargetScanHuman8.0检测靶向DEG的微小RNA(miRNA)。在HCV感染细胞中,两个数据库中的 表达均增加,而 和 ()的表达则降低。在前十大蛋白质中未发现CXCL10、SCGN、H2BC5之间存在直接相互作用。CXCL10是丙型肝炎以及病毒蛋白与细胞因子和细胞因子受体KEGG途径相互作用的成员。H2BC5是病毒致癌KEGG途径的成员。常见DEG靶向的预测重叠miRNA如下:59个以 为估计靶点,22个以 为估计靶点,以及 以 ()为估计靶点。我们的研究使用两个不同的数据库,鉴定了两个数据库中HCV感染细胞中上调或下调的基因以及与这些基因相关的miRNA。本研究为未来研究这些基因是否能够预测HCV预后和HCV相关肝癌的发展奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/c0eb220045a9/genes-15-01502-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/fbe09d4d823f/genes-15-01502-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/2b799db4884c/genes-15-01502-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/fcd9af7089c7/genes-15-01502-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/6d4baa79afe4/genes-15-01502-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/e79826b1f03f/genes-15-01502-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/4bfe1b9350cd/genes-15-01502-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/1216a0ddd3c6/genes-15-01502-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/c0eb220045a9/genes-15-01502-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/fbe09d4d823f/genes-15-01502-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/2b799db4884c/genes-15-01502-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/fcd9af7089c7/genes-15-01502-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/6d4baa79afe4/genes-15-01502-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/e79826b1f03f/genes-15-01502-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/4bfe1b9350cd/genes-15-01502-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/1216a0ddd3c6/genes-15-01502-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16bb/11675613/c0eb220045a9/genes-15-01502-g008.jpg

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