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Emerging evidence suggests that in the tumor microenvironment,\n                  <jats:italic>C. albicans<\/jats:italic>\n                  drives tumor progression in its pathogenic hyphal form with the secretion of its peptide toxin, candidalysin, enhancing tumor cell evolution. CRC cells differentially express transglutaminase 2 (TG2), which mediates covalent binding to\n                  <jats:italic>C. albicans<\/jats:italic>\n                  and can promote tumor adaptability and metastases. However, mechanistic insight into how\n                  <jats:italic>C. albicans<\/jats:italic>\n                  infection leads to CRC progression is incomplete. CRC lines that express high (SW480) and low (LoVo, HCT 116) TG2 were infected with\n                  <jats:italic>C. albicans<\/jats:italic>\n                  and examined for effects on epithelial to mesenchymal transition (EMT) and cell migration. Parallel studies were also conducted using a candidalysin-deficient\n                  <jats:italic>C. albicans<\/jats:italic>\n                  strain.\n                  <jats:italic>C. albicans<\/jats:italic>\n                  invasion stimulated TG2 activity that allowed covalent crosslinking of the hyphae adhesin, Hwp1, to SW480 cells in a candidalysin-dependent manner. Independent of TG2 expression, infection of SW480, LoVo, and HCT 116 cells induced EMT-like changes including downregulation of E-cadherin, altered\n                  <jats:italic>N<\/jats:italic>\n                  -glycosylation of N-cadherin, and variable Snail1 expression. Infection increased MGAT5 activity, which raised levels of branched \u03b2(1-6)\n                  <jats:italic>N<\/jats:italic>\n                  -glycans. Infection promoted CRC cell motility that was blocked by pharmacological inhibition of MGAT5. These findings reveal that\n                  <jats:italic>C. albicans<\/jats:italic>\n                  can promote covalent attachment to TG2-high CRC cells and induce EMT-like and migration-associated changes through TG2-independent alterations in epithelial plasticity and\n                  <jats:italic>N<\/jats:italic>\n                  -glycosylation.\n                <\/jats:p>","DOI":"10.64898\/2026.09.09.750446","type":"posted-content","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T09:40:12Z","timestamp":1789119612000},"source":"Crossref","is-referenced-by-count":0,"title":["<i>Candida albicans<\/i>\n                  promotes self-adhesion and tumor cell progression of colorectal cancer cells"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-7209-9831","authenticated-orcid":false,"given":"Janet F.","family":"Staab","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA"},{"name":"Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia K. 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