{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,18]],"date-time":"2025-06-18T01:35:32Z","timestamp":1750210532804,"version":"3.40.5"},"reference-count":37,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2019,5,2]],"date-time":"2019-05-02T00:00:00Z","timestamp":1556755200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81330044","81772424"],"award-info":[{"award-number":["81330044","81772424"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Congenital scoliosis (CS) is the result of anomalous vertebrae development, but the pathogenesis of CS remains unclear. Long non\u2010coding RNAs (lncRNAs) have been implicated in embryo development, but their role in CS remains unknown. In this study, we investigated the role and mechanisms of a specific lncRNA, SULT1C2A, in somitogenesis in a rat model of vitamin A deficiency (VAD)\u2010induced CS. Bioinformatics analysis and quantitative real\u2010time PCR (qRT\u2010PCR) indicated that SULT1C2A expression was down\u2010regulated in VAD group, accompanied by increased expression of rno\u2010miR\u2010466c\u20105p but decreased expression of <jats:italic>Foxo4<\/jats:italic> and somitogenesis\u2010related genes such as <jats:italic>Pax1<\/jats:italic>, <jats:italic>Nkx3\u20102<\/jats:italic> and <jats:italic>Sox9<\/jats:italic> on gestational day (GD) 9. Luciferase reporter and small interfering RNA (siRNA) assays showed that SULT1C2A functioned as a competing endogenous RNA to inhibit rno\u2010miR\u2010466c\u20105p expression by direct binding, and rno\u2010miR\u2010466c\u20105p inhibited <jats:italic>Foxo4<\/jats:italic> expression by binding to its 3\u2032 untranslated region (UTR). The spatiotemporal expression of SULT1C2A, rno\u2010miR\u2010466c\u20105p and <jats:italic>Foxo4<\/jats:italic> axis was dynamically altered on GDs 3, 8, 11, 15 and 21 as detected by qRT\u2010PCR and northern blot analyses, with parallel changes in Protein kinase B (AKT) phosphorylation and PI3K expression. Taken together, our findings indicate that SULT1C2A enhanced <jats:italic>Foxo4<\/jats:italic> expression by negatively modulating rno\u2010miR\u2010466c\u20105p expression via the PI3K\u2010ATK signalling pathway in the rat model of VAD\u2010CS. Thus, SULT1C2A may be a potential target for treating CS.<\/jats:p>","DOI":"10.1111\/jcmm.14355","type":"journal-article","created":{"date-parts":[[2019,5,2]],"date-time":"2019-05-02T07:27:11Z","timestamp":1556782031000},"page":"4582-4591","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["LncRNA\u2010SULT1C2A regulates <i>Foxo4<\/i> in congenital scoliosis by targeting rno\u2010miR\u2010466c\u20105p through PI3K\u2010ATK signalling"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1824-6116","authenticated-orcid":false,"given":"Chong","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Orthopedic Surgery Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haining","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiaqi","family":"Bi","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Li","sequence":"additional","affiliation":[{"name":"Beijing Zhongke Jingyun Technology Company Ltd. 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