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However, the underlying mechanism is poorly understood. Herein, we investigated the potential mechanism of <jats:italic>H. pylori<\/jats:italic>\u2010induced GKN1 downregulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and methods<\/jats:title><jats:p>GKN1 and AU\u2010rich element RNA\u2010binding factor 1 (AUF1) expressions were assessed by quantitative real\u2010time PCR, Western blot, or immunohistochemistry in <jats:italic>H. pylori<\/jats:italic>\u2010infected tissues and <jats:italic>H. pylori<\/jats:italic> co\u2010cultured cell lines. The regulation of AUF1 on GKN1 was determined by RNA pulldown assay, RNA immunoprecipitation, mRNA turnover, and luciferase activity assays. The involvement of phosphorylated extra\u2010cellular signal\u2010regulated kinase (p\u2010ERK) or CagA in <jats:italic>H. pylori<\/jats:italic>\u2010induced AUF1 expression was verified using p\u2010ERK inhibitor or CagA knockout <jats:italic>H. pylori<\/jats:italic>. In addition, the cell proliferation and migration capacities of <jats:italic>AUF1<\/jats:italic>\u2010knockdown cells were investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>GKN1 expression progressively decreased from <jats:italic>H. pylori<\/jats:italic>\u2010infected gastritis to gastric cancer tissues. <jats:italic>H. pylori<\/jats:italic> co\u2010culture also induced significant GKN1 reduction in GES\u20101 and BGC\u2010823 cells. Besides, the mRNA level of <jats:italic>GKN1<\/jats:italic> and <jats:italic>AUF1<\/jats:italic> in human gastric mucosa showed negative correlation significantly. <jats:italic>AUF1<\/jats:italic> knockdown resulted in upregulation of GKN1 expression and promoted <jats:italic>GKN1<\/jats:italic> mRNA decay by binding the 3\u2032 untranslated region of <jats:italic>GKN1<\/jats:italic> mRNA <jats:italic>H. pylori<\/jats:italic>\u2010induced AUF1 expression was associated with p\u2010ERK activation and CagA. Furthermore, knockdown of <jats:italic>AUF1<\/jats:italic> significantly inhibited cell viability, migration ability, and arrested fewer cells in S\u2010phase.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our data demonstrated that <jats:italic>H. pylori<\/jats:italic> infection downregulated GKN1 expression via the CagA\/p\u2010ERK\/AUF1 pathway. AUF1 promoted gastric cancer at least partly through downregulating GKN1, which presented a novel potential target for the treatment of gastric cancer.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12665","type":"journal-article","created":{"date-parts":[[2019,10,28]],"date-time":"2019-10-28T03:34:47Z","timestamp":1572233687000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["<i>Helicobacter pylori<\/i> inhibits GKN1 expression via the CagA\/p\u2010ERK\/AUF1 pathway"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0668-0620","authenticated-orcid":false,"given":"Yanlei","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Gastroenterology Peking University Third Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Infectious 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