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<p>Epidemiological evidence indicates that <i>HP-I</i> increases the risk of CRC, yet the underlying pathological mechanisms remain unclear. This study aimed to identify DEGs associated with <i>HP-I</i> and CRC by analyzing public RNA sequencing data and to investigate potential molecular pathways. Gene expression profiles of <i>HP-I</i> and CRC were obtained from the GEO and TCGA databases. Shared DEGs were identified, followed by functional annotation, PPI network construction, hub gene identification, and validation of hub gene expression and diagnostic and prognostic value in CRC. Immune infiltration analysis, TFs prediction for hub genes, and potential small-molecule compound screening were also performed. A total of 112 shared DEGs were identified, including 74 up-regulated genes and 38 down-regulated genes. Enrichment analysis indicated that these DEGs were predominantly involved in immune and inflammation-related pathways. Eight hub genes (AGT, CCL20, CXCL1, CXCL2, CXCL5, CXCL9, CXCL10, and MMP9) were identified as central players contributing to the development of comorbid HP-I and CRC. Notably, these genes demonstrated good diagnostic performance in CRC, with AUC values ranging from 0.682 to 0.933. CXCL1 and CXCL9 were identified as prognostic markers for CRC. Immune infiltration analysis revealed a significant dysregulation of CD4⁺ T cell subsets in the context of HP-I and CRC. Finally, DY-131 was identified as a potential therapeutic candidate through the CMap database. This study reveals the potential common molecular mechanisms between <i>HP-I</i> and CRC, identifies shared hub genes, and highlights candidate therapeutic compounds.</p>

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Common crosstalk genes and molecular mechanisms in Helicobacter pylori infection and colorectal cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月26日

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  • Na Wei,
  • Yao-Hui Ma,
  • Ling-Zhu Gou,
  • Tong Lu,
  • Xinglan Chen,
  • Dekui Zhang

摘要

Epidemiological evidence indicates that HP-I increases the risk of CRC, yet the underlying pathological mechanisms remain unclear. This study aimed to identify DEGs associated with HP-I and CRC by analyzing public RNA sequencing data and to investigate potential molecular pathways. Gene expression profiles of HP-I and CRC were obtained from the GEO and TCGA databases. Shared DEGs were identified, followed by functional annotation, PPI network construction, hub gene identification, and validation of hub gene expression and diagnostic and prognostic value in CRC. Immune infiltration analysis, TFs prediction for hub genes, and potential small-molecule compound screening were also performed. A total of 112 shared DEGs were identified, including 74 up-regulated genes and 38 down-regulated genes. Enrichment analysis indicated that these DEGs were predominantly involved in immune and inflammation-related pathways. Eight hub genes (AGT, CCL20, CXCL1, CXCL2, CXCL5, CXCL9, CXCL10, and MMP9) were identified as central players contributing to the development of comorbid HP-I and CRC. Notably, these genes demonstrated good diagnostic performance in CRC, with AUC values ranging from 0.682 to 0.933. CXCL1 and CXCL9 were identified as prognostic markers for CRC. Immune infiltration analysis revealed a significant dysregulation of CD4⁺ T cell subsets in the context of HP-I and CRC. Finally, DY-131 was identified as a potential therapeutic candidate through the CMap database. This study reveals the potential common molecular mechanisms between HP-I and CRC, identifies shared hub genes, and highlights candidate therapeutic compounds.