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

Figure 4 Knockdown of epidermal growth factor receptor kinase substrate 8-like protein 3 inhibits proliferation, migration, and invasion of gastric cancer cells in vitro. A: Western blot analysis confirmed efficient epidermal growth factor receptor kinase substrate 8-like protein 3 (EPS8L3) knockdown; sh1 and sh2 demonstrated the knockdown efficacy; B and C: Colony formation assays showed a significant reduction in colony formation upon EPS8L3 knockdown; D and E: Edu assays demonstrated a marked decrease in cell proliferation in AGS and SGC-7901 cells upon EPS8L3 knockdown; F and G: Transwell assays indicated a significant reduction in invasion and migration in AGS (F) and SGC-7901 (G) cells with EPS8L3 knockdown; H and I: Cell scratch assays revealed decreased migration capacity in AGS (H) and SGC-7901 (I) cells following EPS8L3 silencing. Data are shown as the mean ± SD (n = 3). ^bP < 0.01 vs negative control group, ^cP < 0.001 vs negative control group. EPS8L3: Epidermal growth factor receptor kinase substrate 8-like protein 3; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; NC: Negative control.