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<p>Sodium butyrate (NaB), a histone deacetylase inhibitor, can induce lytic replication of Epstein-Barr virus (EBV). This study aimed to investigate the potential role of EBV reactivation in tumorigenic mechanisms in EBV-associated gastric cancer (EBVaGC) by activating EBV lytic replication using NaB. AGS cells (EBV-negative) and AGS-EBV cells (EBV-positive) were treated with NaB for 12 and 24&#xa0;h, followed by transcriptomic sequencing to obtain host gene expression profiles. Three groups of differentially expressed genes (DEGs) were identified: Control vs. NaB 12&#xa0;h (813 DEGs), Control vs. NaB 24&#xa0;h (1243 DEGs), and Control vs. NaB combining 12&#xa0;h and 24&#xa0;h (1528 DEGs). GO and KEGG analyses revealed that these DEGs were significantly enriched in EBV infection, immune-inflammatory pathways (such as TNF and NF-κB signaling), and cancer-related pathways, indicating that EBV lytic activation triggers these signaling events and induces a strong host immune response along with carcinogenic effects. A protein-protein interaction (PPI) network was constructed and imported into Cytoscape, and the cytoHubba plugin was used to screen for hub genes. Seven consensus hub genes (TLR2, IL1A, CSF1, PECAM1, CXCL10, CD4, CD34) were identified by intersecting the results from different algorithms, and their mRNA expression levels were validated by qRT-PCR. Notably, only CXCL10 expression was consistent with the transcriptomic sequencing results, suggesting that under the conditions of EBV infection and NaB treatment, CXCL10 may play a crucial role in the biological responses of host cells, providing important clues for exploring the mechanism of EBV infection and identifying the targets of NaB.</p>

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The mechanism of NaB-activated lytic replication of EBV and its hub genes in transcriptome regulation of gastric cancer cells

  • 期刊论文

  • 发表日期：

    2026年6月26日

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  • Yuying Chen,
  • Zhaoxin Tian,
  • Zhiyuan Gong,
  • Wen Liu,
  • Bing Luo

摘要

Sodium butyrate (NaB), a histone deacetylase inhibitor, can induce lytic replication of Epstein-Barr virus (EBV). This study aimed to investigate the potential role of EBV reactivation in tumorigenic mechanisms in EBV-associated gastric cancer (EBVaGC) by activating EBV lytic replication using NaB. AGS cells (EBV-negative) and AGS-EBV cells (EBV-positive) were treated with NaB for 12 and 24 h, followed by transcriptomic sequencing to obtain host gene expression profiles. Three groups of differentially expressed genes (DEGs) were identified: Control vs. NaB 12 h (813 DEGs), Control vs. NaB 24 h (1243 DEGs), and Control vs. NaB combining 12 h and 24 h (1528 DEGs). GO and KEGG analyses revealed that these DEGs were significantly enriched in EBV infection, immune-inflammatory pathways (such as TNF and NF-κB signaling), and cancer-related pathways, indicating that EBV lytic activation triggers these signaling events and induces a strong host immune response along with carcinogenic effects. A protein-protein interaction (PPI) network was constructed and imported into Cytoscape, and the cytoHubba plugin was used to screen for hub genes. Seven consensus hub genes (TLR2, IL1A, CSF1, PECAM1, CXCL10, CD4, CD34) were identified by intersecting the results from different algorithms, and their mRNA expression levels were validated by qRT-PCR. Notably, only CXCL10 expression was consistent with the transcriptomic sequencing results, suggesting that under the conditions of EBV infection and NaB treatment, CXCL10 may play a crucial role in the biological responses of host cells, providing important clues for exploring the mechanism of EBV infection and identifying the targets of NaB.