{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T13:12:31Z","timestamp":1778591551501,"version":"3.51.4"},"reference-count":33,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2021,6,9]],"date-time":"2021-06-09T00:00:00Z","timestamp":1623196800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Obstet and Gynaecol"],"published-print":{"date-parts":[[2021,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Recurrent miscarriage (RM) is a distressing reproductive issue worldwide. Dysfunction of trophoblasts can trigger numerous unfavorable pregnant outcomes such as RM, stillbirth, and fetal malformation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this text, the roles and molecular basis of long non\u2010coding RNA insulin growth factor 2 antisense (IGF2\u2010AS) in the development of trophoblast cells were further investigated. IGF2\u2010AS, microRNA\u2010520g (miR\u2010520g), and N\u2010cadherin levels were measured by RT\u2010qPCR assay. Cell viability, the number of colonies, cell apoptosis, migration, and invasion were measured by CCK\u20108 assay, colony formation assay, flow cytometry, transwell migration, and invasion assays, respectively. The relative proteins expression was detected by western blot.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The interaction between miR\u2010520g and IGF2\u2010AS or N\u2010cadherin was tested by bioinformatics prediction analysis, and confirmed by dual\u2010luciferase reporter assay, RNA pull\u2010down assay, and RNA immunoprecipitation (RIP) assay. Our data revealed that IGF2\u2010AS and N\u2010cadherin levels were notably decreased, and miR\u2010520g was strikingly increased in the placentas from RM patients. IGF2\u2010AS overexpression promoted cell proliferation, migration, invasion, epithelial\u2010mesenchymal transition (EMT), and hampered cell apoptosis in trophoblast cells, while IGF2\u2010AS deletion exhibited opposite results. Moreover, miR\u2010520g was a target gene of IGF2\u2010AS and negatively regulated by IGF2\u2010AS. MiR\u2010520g inhibitor enhanced the proliferation, migration, and invasion capability of trophoblast cells, suppressed cell apoptosis, and promoted the EMT process. Moreover, the effects of IGF2\u2010AS overexpression on trophoblast cells were reversed by miR\u2010520g upregulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings indicated that IGF2\u2010AS facilitated trophoblast cell proliferation, migration, invasion, EMT, and suppressed cell apoptosis by regulating miR\u2010520g\/N\u2010cadherin axis, providing potential biomarkers for RM.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jog.14886","type":"journal-article","created":{"date-parts":[[2021,6,10]],"date-time":"2021-06-10T00:29:37Z","timestamp":1623284977000},"page":"3047-3059","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Long non\u2010coding <scp>RNA IGF2\u2010AS<\/scp> promotes trophoblast cell proliferation, migration, and invasion by regulating <scp>miR<\/scp>\u2010520g\/N\u2010cadherin 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