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

Figure 6 Relationship between the expression level of epidermal growth factor receptor kinase substrate 8-like protein 3 and indicators related to ferroptosis in gastric cancer. A: Kyoto Encyclopedia of Genes and Genomes analysis showed that the expression level of epidermal growth factor receptor kinase substrate 8-like protein 3 (EPS8L3) in gastric cancer (GC) was significantly correlated with glutathione metabolism; B and C: Western blot results showed that knockdown of EPS8L3 in GC cells significantly reduced the protein levels of solute carrier family 7 member 11 and glutathione peroxidase 4, and the opposite was true for overexpression of EPS8L3; D: Flow assay of reactive oxygen species levels showed that knockdown of EPS8L3 in GC cells significantly increased intracellular reactive oxygen species levels, and the opposite was true for overexpression of EPS8L3; E: Malondialdehyde assay results indicated that knockdown of EPS8L3 significantly increased malondialdehyde levels in GC cells (AGS and SGC-7901), and the opposite was true for overexpression of EPS8L3; F: Co-immunoprecipitation assay demonstrating a direct interaction between EPS8L3 and both solute carrier family 7 member 11 and glutathione peroxidase 4. Data are shown as the mean ± SD (n = 3). ^aP < 0.05 vs negative control group, ^bP < 0.01 vs negative control group, ^cP < 0.001 vs negative control group. SLC7A11: Solute carrier family 7 member 11; GPX4: Glutathione peroxidase 4; EPS8L3: Epidermal growth factor receptor kinase substrate 8-like protein 3; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; NC: Negative control; MDA: Malondialdehyde; OE: Overexpression.