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Biol."],"abstract":"<jats:p>Transcoelomic spread of serous ovarian cancer (SOC) results from the cooperative interactions between cancer and host components. Tumor-derived factors might allow the conversion of mesothelial cells (MCs) into tumor-associated MCs, providing a favorable environment for SOC cell dissemination. However, factors and molecular mechanisms involved in this process are largely unexplored. Here we investigated the tumor-related endothelin-1 (ET-1) as an inducer of changes in MCs supporting SOC progression. Here, we report a significant production of ET-1 from MCs associated with the expression of its cognate receptors, ET<jats:sub>A<\/jats:sub> and ET<jats:sub>B<\/jats:sub>, along with the protein \u03b2-arrestin1. ET-1 triggers MC proliferation via \u03b2-arrestin1-dependent MAPK and NF-kB pathways and increases the release of cancer-related factors. The ET<jats:sub>A<\/jats:sub>\/ET<jats:sub>B<\/jats:sub> receptor activation supports the genetic reprogramming of mesothelial-to-mesenchymal transition (MMT), with upregulation of mesenchymal markers, as fibronectin, \u03b1-SMA, N-cadherin and vimentin, NF-kB-dependent Snail transcriptional activity and downregulation of E-cadherin and ZO-1, allowing to enhanced MC migration and invasion, and SOC transmesothelial migration. These effects are impaired by either blockade of ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R or by \u03b2-arrestin1 silencing. Notably, in peritoneal metastases both ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R are co-expressed with MMT markers compared to normal control peritoneum. Collectively, our report shows that the ET-1 axis may contribute to the early stage of SOC progression by modulating MC pro-metastatic behaviour via MMT.<\/jats:p>","DOI":"10.3389\/fcell.2021.764375","type":"journal-article","created":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T00:11:06Z","timestamp":1638403866000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Ovarian Cancer-Driven Mesothelial-to-Mesenchymal Transition is Triggered by the Endothelin-1\/\u03b2-arr1 Axis"],"prefix":"10.3389","volume":"9","author":[{"given":"Danila","family":"Del Rio","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilenia","family":"Masi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Caprara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesca","family":"Spadaro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flavia","family":"Ottavi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raffaele","family":"Strippoli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pilar","family":"Sandoval","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"L\u00f3pez-Cabrera","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricardo","family":"Sainz de la Cuesta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Bagnato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Rosan\u00f2","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,12,1]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"256","DOI":"10.3389\/fonc.2013.00256","article-title":"Getting to Know Ovarian Cancer Ascites: Opportunities for Targeted Therapy-Based Translational Research","volume":"3","author":"Ahmed","year":"2013","journal-title":"Front. 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