Helicobacter pylori promotes gastric cancer progression by upregulating EPS8L3 to inhibit ferroptosis

Figure 2 Helicobacter pylori infection increases epidermal growth factor receptor kinase substrate 8-like protein 3 expression. A and B: Heatmap (A) and volcano plot (B) displaying the overall transcriptomic changes in AGS cells after Helicobacter pylori (H. pylori) infection, with epidermal growth factor receptor kinase substrate 8-like protein 3 (EPS8L3) significantly upregulated among the differentially expressed genes; C: Gene Set Enrichment Analysis enrichment analysis of RNA-seq data revealed that H. pylori infection activates the nuclear factor kappa-B (NF-κB) signaling pathway; D: The GEPIA database showed a significant correlation between EPS8L3 and NF-κB; E-G: Protein levels of EPS8L3 and NF-κB increased in GES-1, AGS, and MKN45 cells over time in co-culture with H. pylori; H: Immunohistochemical analysis revealed a significantly higher level of EPS8L3 expression in tumor tissues from H. pylori-positive gastric cancer patients compared to those from H. pylori-negative patients. Data are shown as the mean ± SD (n = 3). ^aP < 0.05 vs control, ^bP < 0.01 vs control, ^cP < 0.001 vs control. NF-κB: Nuclear factor kappa-B; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase.