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ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Bacteria and Host
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1582131
Helicobacter pylori Induced miR-362-5p Upregulation Drives Gastric Cancer Progression and Links Hepatocellular Carcinoma through an Exosome-Dependent Pathway
Provisionally accepted
Huilin Zhao*
Jianhui Zhang
Liu ShuzhenJuan ZhangMingzhu FengShu ChenYinuo ZhangZekun SunXinying CaoChao GaoXiaofei Ji- School of Basic Medical Sciences, Binzhou Medical University, Yantai, Shandong Province, China
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Helicobacter pylori (H. pylori) infection serves as a major risk factor for gastric cancer (GC), with dysregulated miRNA profiles playing a pivotal role in the disease's progression. This study highlighted a significant upregulation of miR-362-5p in GC tissues associated with H. pylori infection. Downregulation of miR-362-5p in GC cells impeded proliferation and migration in vitro and suppressed tumor growth in vivo, counteracting H. pylori-induced carcinogenesis. Bioinformatics analysis and luciferase assays identified TLE4 as a direct target of miR-362-5p, unveiling a TLE4dependent mechanism through which miR-362-5p promotes GC progression. The miR-362-5p/TLE4 axis was further implicated in H. pylori-driven neoplastic transformations in GC cells. Exosomemediated transport of miR-362-5p, induced by H. pylori, was found to be absorbed by GC cells and detected at elevated levels in the serum of infected mice. Fluorescent labeling revealed the systemic distribution of miR-362-5p-encompassing exosomes, particularly within liver cells. These exosomes elevated intracellular miR-362-5p, thereby enhancing hepatocellular carcinoma cell proliferation and migration by targeting TLE4, establishing a link between H. pylori infection and liver cancer development. In summary, H. pylori infection upregulates miR-362-5p, facilitating GC progression via TLE4 targeting, while exosome-mediated transfer amplifies its effects, potentially contributing to hepatocarcinogenesis.
Keywords: Helicobacter pylori, MiR-362-5p, Tle4, gastric cancer, Exosomes, Hepatocellular Carcinoma
Received: 24 Feb 2025; Accepted: 14 Apr 2025.
Copyright: © 2025 Zhao, Zhang, Shuzhen, Zhang, Feng, Chen, Zhang, Sun, Cao, Gao and Ji. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Huilin Zhao, School of Basic Medical Sciences, Binzhou Medical University, Yantai, 264003, Shandong Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.