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The objective of the present study was to determine if the knockdown of MIAT in fibroid xenografts will increase miR-29 levels and reduce the expression of genes targeted by this miRNA such as collagen and cell cycle regulatory proteins in a mouse model for fibroids. Ovariectomized CB-17 SCID\/Beige mice bearing estrogen\/progesterone pellets were implanted subcutaneously in the flank with equal weight of fibroid explants which had been transduced by lentivirus for either control (empty vector) or MIAT knockdown for four weeks (n=7). Knockdown of MIAT in fibroid xenografts resulted in a 30% reduction of tumor weight and a marked increase in miR-29a, -b, and -c levels in the xenografts. There was reduced cell proliferation and expression of cell cycle regulatory genes CCND1, CDK2, and E2F1 and no significant changes in apoptosis. The xenografts with MIAT knockdown expressed lower mRNA and protein levels of FN1, COL3A1, and TGF-\u03b23, and total collagen protein. Targeting MIAT, which sponges the pro-fibrotic miR-29 family, is an effective therapy for fibroids by reducing cell proliferation and thereby, tumor growth and accumulation of ECM, which is a hallmark of these benign gynecologic tumors.<\/jats:p>","DOI":"10.1042\/cs20240190","type":"journal-article","created":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T05:39:27Z","timestamp":1717133967000},"page":"699-709","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Targeting the long non-coding RNA MIAT for the treatment of fibroids in an animal model"],"prefix":"10.1042","volume":"138","author":[{"given":"Tsai-Der","family":"Chuang","sequence":"first","affiliation":[{"name":"1Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, CA, U.S.A."},{"name":"2The Lundquist Institute for Biomedical Innovation, Torrance, CA, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nhu","family":"Ton","sequence":"additional","affiliation":[{"name":"2The Lundquist Institute for Biomedical Innovation, Torrance, CA, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathaly","family":"Manrique","sequence":"additional","affiliation":[{"name":"2The Lundquist Institute for Biomedical Innovation, Torrance, CA, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shawn","family":"Rysling","sequence":"additional","affiliation":[{"name":"2The Lundquist Institute for Biomedical Innovation, Torrance, CA, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4996-5762","authenticated-orcid":false,"given":"Omid","family":"Khorram","sequence":"additional","affiliation":[{"name":"1Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, CA, U.S.A."},{"name":"2The Lundquist Institute for Biomedical Innovation, Torrance, CA, U.S.A."},{"name":"3Department of Obstetrics and Gynecology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA, U.S.A."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2024,6,7]]},"reference":[{"key":"2024061108313454700_B1","doi-asserted-by":"publisher","first-page":"1297","DOI":"10.1152\/physrev.00041.2015","article-title":"Non-coding RNAs in development and disease: background, mechanisms, and therapeutic approaches","volume":"96","author":"Beermann","year":"2016","journal-title":"Physiol. 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