Identification and validation of top differentially expressed genes in H. pylori-associated gastric cancer

Helicobacter pylori infection is a key environmental risk factor implicated in the pathogenesis and progression of gastric cancer. However, the molecular mechanisms linking H. pylori colonization to key tumor-related gene expression remain incompletely defined. This study aimed to investigate the differential expression of fibrinogen gamma chain (FGG), fibrinogen alpha chain (FGA), baculoviral IAP repeat containing 3 (BIRC3), mucin 4 (MUC4), and interleukin 24 (IL24) in gastric cancer tissues stratified by H. pylori infection status. This study utilized the publicly available GSE70394 dataset to identify differentially expressed genes by comparing gene expression profiles between H. pylori-infected cells with and without treatment. Subsequently, the expression of the identified candidate genes was evaluated in gastric cancer tissue samples stratified according to H. pylori infection status (positive versus negative). Gastric tumor tissue samples were obtained from patients with histopathologically confirmed intestinal-type gastric adenocarcinoma. H. pylori infection status was determined using the rapid urease test (RUT), and patients were classified as H. pylori-positive or H. pylori-negative accordingly. Quantitative real-time PCR (qRT-PCR) was performed to assess the expression levels of the selected genes. Gene expression levels were subsequently compared between the H. pylori-positive and H. pylori-negative groups using appropriate statistical analyses. FGG and FGA exhibited elevated expression in H. pylori-positive gastric cancer tissues relative to H. pylori-negative cases, consistent with enhanced inflammation and pro-thrombotic microenvironment in infection-associated tumors. BIRC3 was significantly upregulated in the H. pylori-positive group, supporting a role for apoptosis inhibition in infection-driven carcinogenesis. MUC4 expression was downregulated in H. pylori-associated cancers, implicating mucosal barrier disruption in tumor progression. IL24 moderately increased expression in H. pylori-positive tumors, suggesting a potential but less pronounced role in immune modulation. These findings support an association between H. pylori infection and specific transcriptional alterations in gastric cancer tissues. Further studies using larger independent cohorts, protein-level validation, and functional approaches are needed to determine the reproducibility, biological significance, and potential clinical relevance of these associations.