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Evidence indicates that CFTR loss\u2010of\u2010function, in addition to promoting a pro\u2010inflammatory phenotype, is associated with an increased risk of developing cancer, suggesting that CFTR can exert tumor\u2010suppressor functions. Three\u2010dimensional (3D)\n                    <jats:italic>in vitro<\/jats:italic>\n                    culture models, such as the CF lung airway\u2010on\u2010a\u2010chip, can be suitable for studying PMN recruitment, as well as events of cancerogenesis, that is epithelial cell invasion and migration, in CF. To gather insight into the pathobiology of CFTR loss\u2010of\u2010function, we generated CFTR\u2010knockout (KO) clones of the 16HBE14o\u2010 human bronchial cell line by CRISPR\/Cas9 gene editing, and performed a comparative proteomic analysis of these clones with their wild\u2010type (WT) counterparts. Systematic signaling pathway analysis of CFTR\u2010KO clones revealed modulation of inflammation, PMN recruitment, epithelial cell migration, and epithelial\u2013mesenchymal transition. Using a latest\u2010generation organ\u2010on\u2010a\u2010chip microfluidic platform, we confirmed that CFTR\u2010KO enhanced PMN recruitment and epithelial cell invasion of the endothelial layer. Thus, a dysfunctional CFTR affects multiple pathways in the airway epithelium that ultimately contribute to sustained inflammation and cancerogenesis in CF.\n                  <\/jats:p>","DOI":"10.1111\/febs.70050","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T23:41:49Z","timestamp":1741736509000},"page":"5086-5104","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Inflammation and epithelial\u2013mesenchymal transition in a\n                    <scp>CFTR<\/scp>\n                    \u2010depleted human bronchial epithelial cell line revealed by proteomics and human organ\u2010on\u2010a\u2010chip"],"prefix":"10.1111","volume":"292","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2149-2855","authenticated-orcid":false,"given":"Domenico","family":"Mattoscio","sequence":"first","affiliation":[{"name":"Department of Medical, Oral and Biotechnological Sciences \u201cG. 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