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By attaching to the gastric epithelium, it triggers signaling pathways that lead to effects ranging from apoptosis to cell proliferation.\n                    <jats:italic>H.\u2009pylori<\/jats:italic>\n                    has been shown to promote nuclear translocation of \u03b2\u2010catenin, inducing gene expression related to the cell cycle. However, recent studies indicate it also causes cell cycle arrest by stabilizing hypoxia\u2010inducible factor 1\u2010alpha (HIF\u20101\u03b1). The mechanisms underlying these opposing effects remain unknown. Here, we explored the effects of\n                    <jats:italic>H.\u2009pylori<\/jats:italic>\n                    infection on \u03b2\u2010catenin and transcription factor 7\u2010like 2 (TCF7L2, also known as TCF\u20104) interaction, as well as downstream transcriptional activity. We observed that, despite maintaining total and nuclear levels of \u03b2\u2010catenin and TCF\u20104, bacterial infection disassembled the \u03b2\u2010catenin\/TCF\u20104 complex, as shown by co\u2010localization and co\u2010immunoprecipitation assays. These changes were followed by decreased TCF\/lymphoid enhancer\u2010binding factor (Lef)\u2010dependent transcription and reduced cell proliferative capacity. Conversely,\n                    <jats:italic>H.\u2009pylori<\/jats:italic>\n                    promoted the association of \u03b2\u2010catenin and HIF\u20101\u03b1 in a protein complex that enhanced transcription of hypoxia response elements. Inhibition of HIF\u20101\u03b1 prevented this association and preserved \u03b2\u2010catenin\/TCF\u20104 interaction, restoring TCF\/Lef\u2010dependent activity. The requirement of HIF\u20101\u03b1 was further confirmed by short hairpin RNA (shRNA) and by using a urease mutant strain unable to stabilize HIF\u20101\u03b1. Interestingly, infection was associated with upregulation of HIF\u20101\u03b1 target genes involved in migration and invasion. Consequently,\n                    <jats:italic>H.\u2009pylori<\/jats:italic>\n                    increased cell invasion while decreasing cell proliferative capacity in a HIF\u20101\u03b1\u2010dependent manner. Thus, our results demonstrate that\n                    <jats:italic>H.\u2009pylori<\/jats:italic>\n                    decreases cell proliferation by reducing \u03b2\u2010catenin\/TCF\u20104 interaction, while increasing \u03b2\u2010catenin\/HIF\u20101\u03b1 complex formation, which is associated with cell invasion as an adaptive mechanism.\n                  <\/jats:p>","DOI":"10.1111\/febs.70179","type":"journal-article","created":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T08:29:28Z","timestamp":1751876968000},"page":"5769-5788","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<i>Helicobacter pylori<\/i>\n                    infection promotes the formation of the \u03b2\u2010catenin\/\n                    <scp>HIF<\/scp>\n                    \u20101\u03b1 complex, enabling adaptive responses in gastric cancer cells"],"prefix":"10.1111","volume":"292","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-5515-0903","authenticated-orcid":false,"given":"H\u00e9ctor A.","family":"Tapia","sequence":"first","affiliation":[{"name":"Institute for Research in Dental Sciences, Faculty of Dentistry Universidad de Chile  Santiago Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (MIII) Universidad de Chile  Santiago Chile"},{"name":"Advanced Center for Chronic Diseases (ACCDiS) Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Camila","family":"Garc\u00eda\u2010Navarrete","sequence":"additional","affiliation":[{"name":"Advanced Scientific Equipment Network (REDECA), Facultad de Medicina Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricio","family":"Silva","sequence":"additional","affiliation":[{"name":"Institute for Research in Dental Sciences, Faculty of Dentistry Universidad de Chile  Santiago Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (MIII) Universidad de Chile  Santiago Chile"},{"name":"Advanced Center for Chronic Diseases (ACCDiS) Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joaqu\u00edn","family":"Lizana","sequence":"additional","affiliation":[{"name":"Institute for Research in Dental Sciences, Faculty of Dentistry Universidad de Chile  Santiago Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (MIII) Universidad de Chile  Santiago Chile"},{"name":"Advanced Center for Chronic Diseases (ACCDiS) Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla","family":"Fonfach","sequence":"additional","affiliation":[{"name":"Institute for Research in Dental Sciences, Faculty of Dentistry Universidad de Chile  Santiago Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (MIII) Universidad de Chile  Santiago Chile"},{"name":"Advanced Center for Chronic Diseases (ACCDiS) Universidad de Chile  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ignacio","family":"Pezoa\u2010Soto","sequence":"additional","affiliation":[{"name":"Centro de Biolog\u00eda Celular y Biomedicina (CEBICEM) Facultad de Ciencias, Universidad San Sebastian  Santiago Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tania","family":"Flores","sequence":"additional","affiliation":[{"name":"Institute for Research in Dental Sciences, Faculty of Dentistry Universidad de Chile  Santiago Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (MIII) Universidad de Chile  Santiago Chile"},{"name":"Advanced Center for Chronic Diseases (ACCDiS) Universidad de Chile  Santiago Chile"},{"name":"Faculty of Dentistry Universidad de La Frontera  Temuco 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