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However, the mechanisms underlying this evasion have not been fully elucidated. N-Myc and STAT Interactor (NMI) have been identified as key players in host immunosurveillance, including interferon (IFN)-induced cell death signaling pathways. NMI levels are markedly reduced in the stromal cells of human endometriotic lesions due to modulation by the Estrogen Receptor beta\/Histone Deacetylase 8 axis. Knocking down NMI in immortalized human endometrial stromal cells (IHESCs) led to elevated RNA levels of genes involved in cell-to-cell adhesion and extracellular matrix signaling following IFNA treatment. Furthermore, NMI knockdown inhibited IFN-regulated canonical signaling pathways, such as apoptosis mediated by Interferon Stimulated Gene Factor 3 and necroptosis upon IFNA treatment. In contrast, NMI knockdown with IFNA treatment activated non-canonical IFN-regulated signaling pathways that promote proliferation, including \u03b2-Catenin and AKT signaling. Moreover, NMI knockdown in IHESCs stimulated ectopic lesions\u2019 growth in mouse endometriosis models. Therefore, NMI is a novel endometriosis suppressor, enhancing apoptosis and inhibiting proliferation and cell adhesion of endometrial cells upon IFN exposure.<\/jats:p>","DOI":"10.3390\/ijms25158145","type":"journal-article","created":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T06:17:44Z","timestamp":1721974664000},"page":"8145","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["N-Myc and STAT Interactor is an Endometriosis Suppressor"],"prefix":"10.3390","volume":"25","author":[{"given":"Yuri","family":"Park","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoming","family":"Guan","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX 77030, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3692-6756","authenticated-orcid":false,"given":"Sang Jun","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA"},{"name":"Nuclear Receptor, Transcription and Chromatin Biology Program, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2024,7,26]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1244","DOI":"10.1056\/NEJMra1810764","article-title":"Endometriosis","volume":"382","author":"Zondervan","year":"2020","journal-title":"N. Engl. J. Med."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"2807","DOI":"10.1016\/j.cell.2021.04.041","article-title":"Endometriosis: Etiology, pathobiology, and therapeutic prospects","volume":"184","author":"Saunders","year":"2021","journal-title":"Cell"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"436","DOI":"10.1016\/j.jmig.2006.05.009","article-title":"Clinical and quality-of-life outcomes after fertility-sparing laparoscopic surgery with bowel resection for severe endometriosis","volume":"13","author":"Lyons","year":"2006","journal-title":"J. Minim. 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