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

Figure 8 Helicobacter pylori infection promotes gastric cancer progression through epidermal growth factor receptor kinase substrate 8-like protein 3-mediated inhibition of ferroptosis. Helicobacter pylori promotes the activation of p-nuclear factor kappa-B and regulates transcription that promotes epidermal growth factor receptor kinase substrate 8-like protein 3 expression. High expression of epidermal growth factor receptor kinase substrate 8-like protein 3 promotes solute carrier family 7 member 11 and glutathione peroxidase 4 by affecting glutathione metabolism, thereby suppressing the occurrence of ferroptosis in cells. NF-κB: Nuclear factor kappa-B; GSH: Glutathione; EPS8L3: Epidermal growth factor receptor kinase substrate 8-like protein 3; GPX4: Glutathione peroxidase 4; ROS: Reactive oxygen species.