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Herein, we investigated Nectin\u20102 in ovarian cancer patients and in cell culture. Tumor as well as peritoneal biopsies of 60 ovarian cancer patients and 22 controls were dual stained for Nectin\u20102 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>31 using immunohistochemistry. Gene expression of Nectin\u20102 was quantified by real\u2010time <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and differences analyzed in relation to various tumor characteristics. In the serum of patients, vascular endothelial growth factor (<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>) was quantified by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>. Effect of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> on Nectin\u20102 expression as well as permeability was investigated in <jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>. In tumor biopsies, Nectin\u20102 protein was mainly localized in tumor cells, whereas in peritoneal biopsies, clear colocalization was found in the vasculature. T3 patients had a significantly higher percentage of positive lymph nodes and this correlated with survival. Nectin\u20102 was significantly upregulated in tumor biopsies in patients with lymph node metastasis and with residual tumor &gt;1\u00a0cm after surgery. Nectin\u20102 expression was significantly suppressed in the peritoneal endothelium of patients associated with significantly increased <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> serum levels. In cell culture, <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> stimulation led to a significant downregulation of Nectin\u20102 which was reversed by <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\u2010inhibition. In addition, Nectin\u20102 knockdown in endothelial cells was associated with significantly increased endothelial permeability. Nectin\u20102 expression in ovarian cancer may support tumor cell adhesion, leading to growth and lymph node metastasis. In addition, <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>\u2010induced Nectin\u20102 suppression in peritoneal endothelium may support an increase in vascular permeability leading to ascites production.<\/jats:p>","DOI":"10.1111\/cas.13992","type":"journal-article","created":{"date-parts":[[2019,3,7]],"date-time":"2019-03-07T14:03:48Z","timestamp":1551967428000},"page":"1872-1882","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Nectin\u20102 in ovarian cancer: How is it expressed and what might be its functional role?"],"prefix":"10.1111","volume":"110","author":[{"given":"Inga","family":"Bekes","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Ulm  Ulm Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanja","family":"L\u00f6b","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology 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