ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Helicobacter pylori-Induced Persistent IGF2BP1 Activation Promotes Ferroptosis Resistance in Gastric Tumorigenesis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Helicobacter pylori (H. pylori) infection is a major risk factor for gastric cancer, yet how a transient bacterial insult induces durable oncogenic reprogramming in gastric epithelial cells remains incompletely understood. Here, we identify insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) as a key mediator of sustained ferroptosis resistance during gastric tumorigenesis. We show that H. pylori infection induces IGF2BP1 expression in gastric epithelial cells, murine models, and human gastric tissues, and that IGF2BP1 upregulation can persist following bacterial eradication, consistent with a potential "hit-and-run"-like mode of epithelial reprogramming. Functionally, sustained IGF2BP1 expression promotes malignant cell survival and tumor growth by suppressing oxidative stress and ferroptosis. Mechanistically, IGF2BP1 functions as an N
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