{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T01:35:40Z","timestamp":1769823340684,"version":"3.49.0"},"reference-count":48,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"vor","delay-in-days":27,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100013306","name":"National Institute of Science Education and Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100013306","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001502","name":"Department of Atomic Energy, Government of India","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001502","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2026,1]]},"abstract":"ABSTRACT<\/jats:title>\n \n \n Helicobacter pylori<\/jats:italic>\n <\/jats:styled-content>\n poses a significant risk for gastric cancer (GC) development.\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n exploits carcinoembryonic antigen\u2010related cell adhesion molecules (CEACAMs) on GC cells (GCCs) to colonise the gastric epithelium. CEACAM1, CEACAM5 and CEACAM6 are known to interact with\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n . We explored the role of\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n in altering CEACAM levels in GCCs and the paracrine effect of infected GCCs on neighbouring uninfected GCCs and macrophages.\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n significantly upregulated CEACAM6. Elevated CEACAM6 in GCCs promoted cell proliferation, cell migration and cell invasion. The effect was further enhanced after infection with\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n . Similarly, soluble factors released by\n CEACAM6<\/jats:italic>\n \u2010transfected GCCs promoted the tumorigenic potential of uninfected GCCs. Macrophages are crucial for GC development and progression. Therefore, it was intriguing to know how CEACAM6 could influence the polarisation of macrophages during\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n infection. To study this, we co\u2010cultured macrophages with either the empty vector or\n CEACAM6<\/jats:italic>\n \u2010expressing GCCs and found that\n \n H. pylori<\/jats:italic>\n <\/jats:styled-content>\n infection increased the M2 polarisation of macrophages co\u2010incubated with\n CEACAM6<\/jats:italic>\n \u2010expressing GCCs. In summary, CEACAM6 was found to promote GC aggressiveness and alter macrophage polarisation. This information could be harnessed to develop future therapeutics for targeting GC.\n <\/jats:p>","DOI":"10.1111\/jcmm.70869","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T12:00:43Z","timestamp":1769601643000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Protumorigenic Responses of\n CEACAM6<\/scp>\n in\n Helicobacter pylori<\/i>\n \u2010Infected Gastric Cancer Cells"],"prefix":"10.1111","volume":"30","author":[{"given":"Debashish","family":"Chakraborty","sequence":"first","affiliation":[{"name":"School of Biological Sciences National Institute of Science Education and Research (NISER) Bhubaneswar, an OCC of Homi Bhabha National Institute Khurda Odisha India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Indrajit","family":"Poirah","sequence":"additional","affiliation":[{"name":"School of Biological Sciences National Institute of Science Education and 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