Helicobacter pylori Infection Is Associated with Increased FGF7 Expression in Gastric Cancer

Helicobacter pylori (Hp) infection is the main risk factor for gastric cancer (GC), promoting malignant transformation via persistent inflammation and oncogenic signaling. Fibroblast growth factor 7 (FGF7) plays a pivotal role in tumor progression; however, its role in Hp-associated GC remains unclear. Differentially expressed genes (DEGs) stratified by Hp status were identified from TCGA and GEO datasets, and core genes were screened using GO, KEGG, and protein – protein interaction analyses. The clinical significance and function of FGF7 were assessed by Cox regression and gene set enrichment analysis (GSEA), with validation in multi-cohort data and in vitro assays. FGF7 was upregulated in Hp-positive samples and associated with poor prognosis. DEGs between high- and low-FGF7 groups were enriched in inflammatory response and epithelial – mesenchymal transition (EMT) pathways, and these findings were validated across cohorts. Correlation analysis showed positive associations between FGF7 and inflammation- and EMT-related genes. qPCR confirmed that Hp infection increased FGF7, IL1R1, and Vimentin mRNA levels. Overall, Hp infection was associated with increased FGF7 expression and inflammatory- and EMT-related molecular changes in GC, suggesting a potential role for FGF7 in Hp-associated gastric carcinogenesis.