{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T13:31:29Z","timestamp":1776691889681,"version":"3.51.2"},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2021,7,30]],"date-time":"2021-07-30T00:00:00Z","timestamp":1627603200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81900500"],"award-info":[{"award-number":["81900500"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81760106"],"award-info":[{"award-number":["81760106"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2021,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p><jats:italic>Helicobacter pylori<\/jats:italic> (<jats:italic>H.\u00a0pylori<\/jats:italic>) is a major risk factor for gastric cancer. The water channel protein Aquaporin 5 (AQP5) is involved in the tumorigenesis and progression of various cancers. In this study, we aimed to explore the role of AQP5 in <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010induced gastric carcinogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>We collected 160 samples which inculded CNAG, IM, Dys and gastric cancer from patients who underwent endoscopy and detected the expression of AQP5. In vivo and vitro <jats:italic>H.\u00a0pylori<\/jats:italic> infection models, we explored the relationship between AQP5 and <jats:italic>H.\u00a0pylori<\/jats:italic>. Plasmid, siRNA and inhibitors were used to investigated the relationship between AQP5 and EMT and the role of AQP5 in <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010induced gastric carcinogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Result<\/jats:title><jats:p>AQP5 expression was gradually increased in human gastric tissues with the progression of chronic nonatrophic gastritis to gastric cancer and associated with the <jats:italic>H.\u00a0pylori<\/jats:italic> infection status. In vivo and in vitro studies showed that <jats:italic>H.\u00a0pylori<\/jats:italic> infection induced AQP5 expression in gastric epithelial cells in a CagA\u2010dependent manner. Knockdown of AQP5 reversed <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010induced cell proliferation and invasion, and \u2010suppressed cell apoptosis. Additionally, knockdown of AQP5 suppressed <jats:italic>H.\u00a0pylori<\/jats:italic>\u2010induced Epithelial\u2010mesenchymal transition (EMT) phenotypes by regulating transcriptional factors, mesenchymal markers, and epithelial markers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We explored the underlying mechanism and our results indicated that knockdown of AQP5 significantly suppressed <jats:italic>H.\u00a0pylori<\/jats:italic> infection\u2010induced phosphorylation of ERK1\/2, MEK and the expression levels of downstream genes. Treatment with an ERK inhibitor suppressed the EMT induced by <jats:italic>H.\u00a0pylori<\/jats:italic> infection. Taken together, this study suggest that pathogenic <jats:italic>H.\u00a0pylori<\/jats:italic> infection promotes AQP5 expression to induce the EMT via the MEK\/ERK signaling pathway.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12842","type":"journal-article","created":{"date-parts":[[2021,7,31]],"date-time":"2021-07-31T05:59:11Z","timestamp":1627711151000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Activation of Aquaporin 5 by carcinogenic <i>Helicobacter pylori<\/i> infection promotes epithelial\u2010mesenchymal transition via the MEK\/ERK pathway"],"prefix":"10.1111","volume":"26","author":[{"given":"Nianshuang","family":"Li","sequence":"first","affiliation":[{"name":"Department of Gastroenterology The First Affiliated Hospital of Nanchang University Nanchang China"},{"name":"Institute of Digestive Disease The First Affiliated Hospital of Nanchang University Nanchang 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