Frontiers in cellular and infection microbiology · 2026
Integrated transcriptomics and molecular docking identify hub genes and statin regulators in Helicobacter pylori-associated gastric mucosal pathogenesis.
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Zhang Minglin, He Xue, Zhao Xuelin, Cai Ting, Liu Xiaoming, Wang Fen
Аннотация
BACKGROUND: Helicobacter pylori (H. pylori), a spiral Gram-negative bacterium colonizing gastric mucosa, damages epithelial cells, driving chronic gastritis, peptic ulcers, and gastric cancer. Mechanisms of its malignant transformation remain unclear.
METHODS: We identified differentially expressed genes (DEGs) and hub genes, pathway enrichment analysis, transcription factors (TFs), small-molecule drug and molecular docking prediction using gastric epithelial cells (GECs) infected with H. pylori strain 26695 and clinical sample datasets.
RESULTS: H. pylori infection of GECs, multiple signaling pathways were activated, including the p53, MAPK, TNF, IL-17, PI3K-Akt and NF-κB signaling, DNA replication, Apoptosis, Cell cycle, Necroptosis. A total of 107 co-expressed DEGs were identified in vitro and in vivo. Using Cytoscape, 20 hub genes were prioritized: TNF, CXCL8, NFKBIA, IRF1, ICAM1, TNFAIP3, BIRC3, CXCL1, ITGAM, RELB, CXCL2, CCL20, NFKB2, EGR1, CDKN1A, IRAK2, JAK1, NFKBIE, TRAF1, and JUNB. These hub genes were enriched in NF-κB, TNF and IL-17 signaling, and responses to bacterial pathogens or lipopolysaccharide. Further analysis identified 9 upregulated TFs: VDR, SPI1, ETS2, STAT1, E2F1, PML, ETS1, BRCA1, MYC, and 4 downregulated TFs: ING4, CEBPD, HSF1, JUN. To explore potential therapeutic interventions, we performed small-molecule drug prediction and molecular docking for hub genes revealed: Simvastatin: Linked to CCL20, NFKBIA, and ICAM1. Atorvastatin: Associated with CDKN1A, ICAM1, and TNF. TPCA-1: Targeting JAK1.
CONCLUSION: These findings provide a theoretical foundation for further investigation into the molecular mechanisms underlying H. pylori-related diseases.
METHODS: We identified differentially expressed genes (DEGs) and hub genes, pathway enrichment analysis, transcription factors (TFs), small-molecule drug and molecular docking prediction using gastric epithelial cells (GECs) infected with H. pylori strain 26695 and clinical sample datasets.
RESULTS: H. pylori infection of GECs, multiple signaling pathways were activated, including the p53, MAPK, TNF, IL-17, PI3K-Akt and NF-κB signaling, DNA replication, Apoptosis, Cell cycle, Necroptosis. A total of 107 co-expressed DEGs were identified in vitro and in vivo. Using Cytoscape, 20 hub genes were prioritized: TNF, CXCL8, NFKBIA, IRF1, ICAM1, TNFAIP3, BIRC3, CXCL1, ITGAM, RELB, CXCL2, CCL20, NFKB2, EGR1, CDKN1A, IRAK2, JAK1, NFKBIE, TRAF1, and JUNB. These hub genes were enriched in NF-κB, TNF and IL-17 signaling, and responses to bacterial pathogens or lipopolysaccharide. Further analysis identified 9 upregulated TFs: VDR, SPI1, ETS2, STAT1, E2F1, PML, ETS1, BRCA1, MYC, and 4 downregulated TFs: ING4, CEBPD, HSF1, JUN. To explore potential therapeutic interventions, we performed small-molecule drug prediction and molecular docking for hub genes revealed: Simvastatin: Linked to CCL20, NFKBIA, and ICAM1. Atorvastatin: Associated with CDKN1A, ICAM1, and TNF. TPCA-1: Targeting JAK1.
CONCLUSION: These findings provide a theoretical foundation for further investigation into the molecular mechanisms underlying H. pylori-related diseases.