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

Figure 5 Helicobacter pylori activates nuclear factor kappa-B to regulate epidermal growth factor receptor kinase substrate 8-like protein 3, inhibition of nuclear factor kappa-B decreases epidermal growth factor receptor kinase substrate 8-like protein 3 expression. A and B: Western blot results showed that in three cell lines (GES-1, AGS, and MKN-45), the nuclear factor kappa-B (NF-κB) inhibitor BAY 11-7082 inhibited the protein levels of NF-κB and p-NF-κB, and the protein levels of epidermal growth factor receptor kinase substrate 8-like protein 3 (EPS8L3) were also reduced by NF-κB and p-NF-κB. The inhibitory effect became more pronounced over time; C: The Jaspar website predicts the NF-κB binding site in the EPS8L3 promoter; D: Chromatin immunoprecipitation assays were performed in AGS cells with p65 transient expression; E and F: Western blot showing that treatment with BAY11-7082 attenuates EPS8L3 overexpression. Data are shown as the mean ± SD (n = 3). ^cP < 0.001 vs control. EPS8L3: Epidermal growth factor receptor kinase substrate 8-like protein 3; NF-κB: Nuclear factor kappa-B; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase.