{"title":"<i>LncRNA BANCR</i> Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the <i>miR-15a-5p</i>/TRIM59 Axis.","authors":"Lixue Liu, Ru Bai, Debang Li, Bai Dai, Ya Tuo","doi":"10.1155/2022/9083822","DOIUrl":null,"url":null,"abstract":"<p><p>Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of <i>long non-coding RNA BRAF-activated non-protein coding RNA</i> (<i>lncRNA BANCR</i>)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating <i>miR-15a-5p</i>/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vimentin expressions in cells. Then, expressions of <i>lncRNA BANCR</i>, <i>microRNA (miR)-15a-5p</i>, and tripartite motif-containing 59 (TRIM59) in tissues and cells were determined by real-time quantitative polymerase chain reaction or Western blot assay, and cell proliferation and invasion were evaluated by cell counting kit-8 and transwell assays. After that, the subcellular localization of <i>lncRNA BANCR</i> and binding of <i>miR-15a-5p</i> to <i>lncRNA BANCR</i> or TRIM59 were analyzed. <i>LncRNA BANCR</i> was upregulated in ectopic endometrial tissues and ectopic ESCs (Ect-ESCs). Silencing <i>lncRNA BANCR</i> suppressed Ect-ESC proliferation and invasion. <i>LncRNA BANCR</i> inhibited <i>miR-15a-5p</i> to promote TRIM59 expression. <i>miR-15a-5p</i> downregulation or TRIM59 overexpression both reversed the effects of silencing <i>lncRNA BANCR</i> on Ect-ESC proliferation and invasion. In summary, our findings suggested that <i>lncRNA BANCR</i> facilitated Ect-ESC proliferation and invasion by inhibiting <i>miR-15a-5p</i> and promoting TRIM59.</p>","PeriodicalId":13988,"journal":{"name":"International Journal of Genomics","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2022-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9576446/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Genomics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1155/2022/9083822","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of long non-coding RNA BRAF-activated non-protein coding RNA (lncRNA BANCR)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating miR-15a-5p/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vimentin expressions in cells. Then, expressions of lncRNA BANCR, microRNA (miR)-15a-5p, and tripartite motif-containing 59 (TRIM59) in tissues and cells were determined by real-time quantitative polymerase chain reaction or Western blot assay, and cell proliferation and invasion were evaluated by cell counting kit-8 and transwell assays. After that, the subcellular localization of lncRNA BANCR and binding of miR-15a-5p to lncRNA BANCR or TRIM59 were analyzed. LncRNA BANCR was upregulated in ectopic endometrial tissues and ectopic ESCs (Ect-ESCs). Silencing lncRNA BANCR suppressed Ect-ESC proliferation and invasion. LncRNA BANCR inhibited miR-15a-5p to promote TRIM59 expression. miR-15a-5p downregulation or TRIM59 overexpression both reversed the effects of silencing lncRNA BANCR on Ect-ESC proliferation and invasion. In summary, our findings suggested that lncRNA BANCR facilitated Ect-ESC proliferation and invasion by inhibiting miR-15a-5p and promoting TRIM59.
期刊介绍:
International Journal of Genomics is a peer-reviewed, Open Access journal that publishes research articles as well as review articles in all areas of genome-scale analysis. Topics covered by the journal include, but are not limited to: bioinformatics, clinical genomics, disease genomics, epigenomics, evolutionary genomics, functional genomics, genome engineering, and synthetic genomics.