Scholarlink

<p>Ferroptosis is an iron-dependent programmed cell death linked to intensified lipid peroxidation reactions, ultimately causing damage to cellular structures such as membranes. It is associated with various viral infections, including Enterovirus 71 (EV71), a major cause of severe hand, foot, and mouth disease with potential neurological complications. However, the role of ferroptosis in EV71 infection is not fully understood. In this study, we downloaded a microarray dataset of EV71-infected samples (GSE71673) from the Gene Expression Omnibus (GEO) and retrieved ferroptosis-related genes (FRGs) from FerrDB. Compared to the control group, we identified 69 differentially expressed ferroptosis-related genes (FR-DEGs) that were differentially expressed in the EV71-infected cell samples compared with the control samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, along with protein‒protein interaction (PPI) network analysis, revealed associations with pathways related to miRNA transcription, protein binding, and cancer. Eight hub genes were identified, with five validated in EV71-infected U87 cells. In the regulatory network, we identified six transcription factors (TFAP2A, STAT3, SP1, EGR1, MAX, and AR) and three microRNAs (hsa-miR-1, hsa-miR-20a, and hsa-miR-545) that play key regulatory roles in the expression of hub genes. In summary, the 5 validated FR-DEGs (IL-6, JUN, CXCL8, FGF2, and TGFB1), six transcription factors and the three microRNAs that regulate hub gene expression. In addition, EV71 infection reduces cellular GSH and GPX4 expression, promotes ROS production, and decreases cell viability. These findings reveal significant transcriptional reprogramming of ferroptosis-associated genes during EV71 infection, highlighting a potential role for this pathway that requires direct experimental validation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Identification of Potential Key Ferroptosis-Related Genes in EV71-Infected Cells Through Bioinformatics Analysis and Experimental Study

  • 期刊论文

  • 发表日期：

    2025年11月25日

查看全文
  • Yuhan Zhang,
  • Meishan Zhou,
  • Liu Yang,
  • Jianing Wang,
  • Xinli Wen,
  • Lu Shi,
  • Yongjuan Liu,
  • Yingying Shi,
  • Liu

摘要

Ferroptosis is an iron-dependent programmed cell death linked to intensified lipid peroxidation reactions, ultimately causing damage to cellular structures such as membranes. It is associated with various viral infections, including Enterovirus 71 (EV71), a major cause of severe hand, foot, and mouth disease with potential neurological complications. However, the role of ferroptosis in EV71 infection is not fully understood. In this study, we downloaded a microarray dataset of EV71-infected samples (GSE71673) from the Gene Expression Omnibus (GEO) and retrieved ferroptosis-related genes (FRGs) from FerrDB. Compared to the control group, we identified 69 differentially expressed ferroptosis-related genes (FR-DEGs) that were differentially expressed in the EV71-infected cell samples compared with the control samples. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, along with protein‒protein interaction (PPI) network analysis, revealed associations with pathways related to miRNA transcription, protein binding, and cancer. Eight hub genes were identified, with five validated in EV71-infected U87 cells. In the regulatory network, we identified six transcription factors (TFAP2A, STAT3, SP1, EGR1, MAX, and AR) and three microRNAs (hsa-miR-1, hsa-miR-20a, and hsa-miR-545) that play key regulatory roles in the expression of hub genes. In summary, the 5 validated FR-DEGs (IL-6, JUN, CXCL8, FGF2, and TGFB1), six transcription factors and the three microRNAs that regulate hub gene expression. In addition, EV71 infection reduces cellular GSH and GPX4 expression, promotes ROS production, and decreases cell viability. These findings reveal significant transcriptional reprogramming of ferroptosis-associated genes during EV71 infection, highlighting a potential role for this pathway that requires direct experimental validation.