Article(id=1291753251704165186, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, articleNumber=PA20260408_OytBZtfl, orderNo=null, doi=10.3969/j.issn.1671-7856.2026.06.002, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753977600000, receivedDateStr=2025-08-01, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785907574821, onlineDateStr=2026-08-05, pubDate=1774800000000, pubDateStr=2026-03-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785907574820, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785907574820, creator=admin, updateTime=1785907574820, updator=admin, issue=Issue{id=1291753151179280707, tenantId=1146029695717560320, journalId=1291416913693474840, year='2026', volume='36', issue='6', pageStart='1', pageEnd='144', issueExtLink='null', onlineDate='null', pubDate='1774800000000', pubDateStr='2026-03-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785907550854, creator='ztmeta', updateTime=1786331902788, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1293533012289941791, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1293533012289941792, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=11, endPage=20, ext={EN=ArticleExt(id=1291753256020104004, articleId=1291753251704165186, tenantId=1146029695717560320, journalId=1291416913693474840, language=EN, title=Mechanism of long-chain non-coding RNA X-inactive specific transcript on the biological behavior of trophoblast cells by targeting the miR-182-5p/HIF-2α molecular axis, columnId=1292760394137887571, journalTitle=Chinese Journal of Comparative Medicine, columnName=Reseaech Reports, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the molecular mechanism by which long-chain non-coding RNA (lncRNA) X-inactive specific transcript (XIST) regulates the biological activity of trophoblast cells. Methods Human HTR-8/Svneo trophoblast cells were cultured in vitro and separated into control, interference empty (transfected with small interfering RNA-normal control (si-NC)), si-XIST-1 (transfected with si-XIST-1), si-XIST-1+anti-NC (co-transfected with si-XIST-1 and anti-NC), and si-XIST-1+anti-182-5p (co-transfected with si-XIST-1 and anti-182-5p) groups. XIST, miR-182-5p, and hypoxia inducible factor-2α (HIF-2α) mRNA expression levels were measured by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) assays. Apoptosis was detected by flow cytometry. Cell migration and invasion abilities were measured by scratch-healing and Transwell experiments. HIF-2α, cleaved-caspase-3, Bcl-2, Bax, matrix metalloproteinase (MMP)-2, and MMP-9 protein levels in cells were measured by Western blot. The targeting relationship of miR-182-5p with XIST and HIF-2α was verified by dualluciferase reporter assay.
Results XIST and HIF-2α mRNA levels, apoptosis rate, and HIF-2α, cleaved-caspase-3, and Bax protein levels in the si-XIST-1 group were lower than those in the control and interference empty groups, while miR-182-5p, cell viability, EdU-positive rate, scratch-healing rate, number of invaded cells, and Bcl-2, MMP-2, and MMP-9 protein levels were higher (P<0.05). HIF-2α mRNA level, apoptosis rate, and HIF-2α, cleaved-caspase-3, and Bax protein levels in the si-XIST-1+anti-182-5p group were higher than those in the si-XIST-1 and si-XIST-1+ anti-NC groups, while miR-182-5p, cell viability, EdU-positive rate, scratch-healing rate, number of invaded cells, and Bcl-2, MMP-2, and MMP-9 protein levels were lower (P<0.05). LncRNA XIST was able to target miR-182-5p in HTR-8/Svneo cells, and HIF-2α was the target of miR-182-5p.
Conclusions Knocking-down lncRNA XIST may inhibit HIF-2α expression by competitively binding to miR-182-5p, thereby enhancing the proliferation, migration, and invasion abilities of HTR-8/Svneo cells and inhibiting cell apoptosis.
, authors=Yan HUANG
1, Linjing ZHANG
1, Honglin WANG
1, Ting ZHANG
1, *, Bo LI
2, authorsList=Yan HUANG, Linjing ZHANG, Honglin WANG, Ting ZHANG, Bo LI, authorCompany=null, correspAuthors=Ting ZHANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291753255940412227, articleId=1291753251704165186, tenantId=1146029695717560320, journalId=1291416913693474840, language=CN, title=lncRNA XIST靶向miR-182-5p/ HIF-2α分子轴对滋养层细胞生物学行为特性影响的机制研究, columnId=1292760394347606213, journalTitle=中国比较医学杂志, columnName=研究报告, runingTitle=null, highlight=null, articleAbstract=
目的 探究长链非编码RNA（lncRNA）X染色体失活特异性转录本（XIST）调控滋养层细胞生物学活性的分子机制。
方法 体外培养人绒毛膜滋养层细胞HTR-8/Svneo，分为对照组、干扰空载组（转染si-NC）和si-XIST-1组（转染si-XIST-1）、si-XIST-1+anti-NC组（共转染si-XIST-1和anti-NC）、si-XIST-1+anti-182-5p组（共转染si-XIST-1和anti-182-5p）。采用RT-qPCR检测细胞中XIST、miR-182-5p和低氧诱导因子2α（HIF-2α） mRNA表达；CCK-8实验和EdU实验检测细胞增殖活力；流式细胞术检测细胞凋亡；划痕愈合实验、Transwell实验检测细胞迁移、侵袭能力；Western blot检测细胞中HIF-2α、cleaved-caspase-3、Bcl-2、Bax、基质金属蛋白（MMP）-2、MMP-9蛋白表达；双荧光素酶报告实验验证miR-182-5p与XIST、HIF-2α的靶向关系。结果与对照组、干扰空载组比较，si-XIST-1组XIST、HIF-2α mRNA水平、凋亡率及HIF-2α、cleaved-caspase-3、Bax蛋白水平降低，miR-182-5p水平、细胞活力、EdU阳性率、划痕愈合率、侵袭细胞数及Bcl-2、MMP-2、MMP-9蛋白水平升高（P< 0.05）；与si-XIST-1组和si-XIST-1+anti-NC组比较，si-XIST-1+ anti-182-5p组HIF-2α mRNA水平、凋亡率及HIF-2α、cleaved-caspase-3、Bax蛋白水平升高，miR-182-5p水平、细胞活力、EdU阳性率、划痕愈合率、侵袭细胞数及Bcl-2、MMP-2、MMP-9蛋白水平降低（P<0.05）。lncRNA XIST可靶向HTR-8/Svneo细胞中的miR-182-5p，HIF-2α是miR-182-5p的靶标。
结论 敲低lncRNA XIST可能是通过竞争性结合miR-182-5p来抑制HIF-2α表达，进而增强HTR-8/Svneo细胞增殖、迁移和侵袭能力，并抑制细胞凋亡。
, authors=黄燕
1, 张林静
1, 汪洪林
1, 张婷
1, *, 李波
2, authorsList=黄燕, 张林静, 汪洪林, 张婷, 李波, authorCompany=null, correspAuthors=张婷, authorNote=
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黄燕（1974—），女，本科，主任医师，研究方向：围产医学。E-mail: hr6050@sina.com
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黄燕（1974—），女，本科，主任医师，研究方向：围产医学。E-mail: hr6050@sina.com
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