山西医科大学学报2025，Vol.56Issue(9)：1057-1066,10.DOI:10.13753/j.issn.1007-6611.2025.09.010
LINC02589通过m6A介导的子宫内膜异位症FTO抑制促进上皮-间充质转化
LINC02589 promotes epithelial-mesenchymal transition via m6A-mediated suppression of FTO in endometriosis
摘要
Abstract
Objective To investigate the expression of long non-coding RNA(lncRNA)LINC02589 and fat mass and obesity-associ-ated protein(FTO)in endometriosis(EMs),and their relationship with m6A methylation levels,and explore the potential roles of LINC02589 and FTO in the pathological process of EMs.Methods Endometrial tissue samples were collected from 10 EMs patients and 10 healthy controls.The expression levels of LINC02589 and FTO were detected by quantitative reverse transcription polymerase chain reaction(qRT-PCR).The m6A methylation level of LINC02589 was assessed using methylated RNA immunoprecipitation fol-lowed by qPCR(MeRIP-qPCR).Protein levels of FTO and m6A were measured by Western blot.Normal endometrial stromal cells(ESCs)were divided into ESCs group and ESCs+17β-estradiol group(ESCs+17β-E).ESCs were divided into Vector+siNC group,Vector+siNC+17β-E group,Vector+siLINC02589+17β-E group,FTO+siNC+17β-E group,and FTO+siLINC02589+17β-E group,and LINC02589 and FTO expression,and m6A methylation levels were detected.Additionally,Western blot was performed to detect FTO,E-cadherin,N-cadherin,and Vimentin protein expressions.Cell migration,invasion,and proliferation were assessed using Transwell and CCK-8 assays.Results Compared to healthy controls,EMs tissues exhibited increased LINC02589 expression(P＜0.001),decreased FTO expression(P＜0.001),and elevated m6A methylation levels(P＜0.001).LINC02589 expression was nega-tively correlated with FTO expression(r=-0.835 9,P＜0.001).Compared to ESCs group,LINC02589 expression and m6A methylation increased in ESCs+17β-E group(P＜0.001),and FTO expression decreased(P＜0.001).Compared to Vector+siNC+17β-E group,m6A methylation levels significantly reduced in Vector+siLINC02589+17β-E group and FTO+siNC+17β-E group(P＜0.001).Com-pared with Vector+siNC+17β-E group,E-cadherin expression increased in FTO+siNC+17β-E group and N-cadherin,Vimentin andβ-catenin expressions decreased(P＜0.001),and the effects were reversed in FTO+siLINC02589+17β-E group(P＜0.001).Functional assays revealed that cell migration,invasion,and proliferation were significantly attenuated in FTO+siNC+17β-E group compared with Vector+siNC+17β-E group(P＜0.01).However,the cellular capabilities were partially restored in FTO+siLINC02589+17β-E group(P＜0.001).Conclusion LINC02589 promotes m6A methylation by negatively regulating FTO expression,thereby mediating estrogen-induced pathogenesis and progression of endometriosis.关键词
子宫内膜异位症/LINC02589/脂肪质量和肥胖相关蛋白/m6A甲基化/雌激素/上皮-间质转化Key words
endometriosis/LINC02589/fat mass and obesity-associated protein/m6A methylation/estrogen/epithelial-mesenchymal transition分类
医药卫生引用本文复制引用
麦虹,罗素芳,廖雁,韦凯伊,杨凤..LINC02589通过m6A介导的子宫内膜异位症FTO抑制促进上皮-间充质转化[J].山西医科大学学报,2025,56(9):1057-1066,10.基金项目
广西壮族自治区卫生健康委员会自筹经费科研课题(Z-A20220651) （Z-A20220651）
