Copyright: ©Author(s) 2026.
World J Gastroenterol. Aug 28, 2026; 32(32): 119744
Published online Aug 28, 2026. doi: 10.3748/wjg.119744
Published online Aug 28, 2026. doi: 10.3748/wjg.119744
Figure 7 Knockdown of epidermal growth factor receptor kinase substrate 8-like protein 3 inhibits tumor growth in in vivo experiments.
A and B: Six nude mice per group were injected with equal amounts of control and sh-epidermal growth factor receptor kinase substrate 8-like protein 3 (EPS8L3) SGC-7901 cells; C and D: Tumor weight (C) and volume (D) profiles indicated that knockdown of EPS8L3 inhibited the proliferation of GC cells in vivo; E: Ki67 staining showing higher expression in the negative control group than in the sh-group in vivo, and hematoxylin and eosin staining showing tumor tissue morphology; F: Representative images of patient-derived gastric cancer organoids showing that growth inhibition by EPS8L3 knockdown is attenuated by Helicobacter pylori co-culture. Data are shown as the mean ± SD (n = 3). bP < 0.05. NC: Negative control.
- Citation: Ma MD, Chen WJ, Yu KX, Wang HZ, Li YX. Helicobacter pylori promotes gastric cancer progression by upregulating EPS8L3 to inhibit ferroptosis. World J Gastroenterol 2026; 32(32): 119744
- URL: https://www.wjgnet.com/1007-9327/full/v32/i32/119744.htm
- DOI: https://dx.doi.org/10.3748/wjg.119744