ArticleCancer medicine2025
Hypoxia and Hypoxia-Reoxygenation Potentiate Helicobacter pylori Infection and Gastric Epithelial Cell Proliferation.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- RHOA-dependent regulation of mitochondrial remodeling and cell motility in hypoxia-exposed gastric epithelial cells.Journal of cell science · 2025Article
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13 authors.
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Abstract
introductionThe gastric epithelium experiences intermittent hypoxia due to various physiological and pathological conditions. However, the impact of hypoxia and hypoxia-reoxygenation of gastric epithelial cells (GECs) on Helicobacter pylori-mediated gastric cancer (GC) has never been investigated. Carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) facilitate H. pylori adhesion onto GECs. We evaluated the effect of hypoxia and hypoxia-reoxygenation on CEACAM6-mediated H. pylori binding, infection, reactive oxygen species (ROS) generation, and GEC proliferation.
methodsHypoxia-inducible factor 1 (HIF1α) and CEACAM6 levels were assessed in various GECs. ROS were measured using 2',7'-dichlorofluorescin diacetate (DCFDA). Bioinformatics analyses were performed to identify the most prominent stomach adenocarcinoma (STAD)-associated NADPH oxidase (NOX) followed by validation by overexpression/suppression studies and western blotting. GC biopsies were examined by immunofluorescence microscopy. Hypoxia-exposed, reoxygenated, or control cells were compared for ROS generation and H. pylori infection. MTT assay determined cell proliferation. RESULTS AND
conclusionsHypoxia and HIF1 mediated upregulation of CEACAM6 in GECs. CEACAM6 significantly promoted ROS generation by inducing NOX4 in hypoxic GECs. HIF1α, CEACAM6, and NOX4 upregulation was detected in gastritis and GC tissues. H. pylori infection significantly increased in hypoxia-exposed GECs as compared to normoxic GECs. Infection of hypoxia-reoxygenated GECs also resulted in significantly increased CEACAM6 and NOX4-mediated ROS generation compared to normoxic GECs. In addition, adhesion of H. pylori, cytotoxin-associated gene A (CagA) translocation, and GEC proliferation were significantly enhanced in hypoxia-reoxygenated GECs. Collectively, this study established that hypoxia and hypoxia-reoxygenation of GECs facilitate H. pylori infection and infection-mediated GEC proliferation.
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