【摘要】 目的 探究子宫内膜异位症(EM)组织中miR-532-3p的表达及其对子宫内膜异位症基质细胞(ESCs)增殖、侵袭和AKT3表达的影响机制。方法 选取2019年11月至2020年3月在廊坊市人民医院行腹腔镜及刮宫术的10例EM患者的异位子宫内膜组织和10例非EM患者的正常子宫内膜组织作为研究对象。从EM患者的异位子宫内膜组织中分离出ESCs,从非EM患者的正常子宫内膜组织中分离出正常子宫内膜间质细胞(NESCs),ESCs中分别转染miR-532-3p-mimic、miR-532-3p-inhibitor及对应的阴性对照进行分组。采用细胞计数试剂盒8(CCK-8)实验、Transwell实验测定细胞的增殖、侵袭能力；采用实时荧光定量聚合酶链反应(qRT-PCR)检测miR-532-3p、AKT3的相对表达水平；采用Western blot检测AKT3的表达；采用双荧光素酶报告基因检测miR-532-3p与AKT3的关系。结果 qRT-PCR结果显示，与正常子宫内膜组织及NESCs相比，异位子宫内膜组织及ESCs中miR-532-3p表达下调(P<0.05)。转染miR-532-3p-mimic的ESCs中miR-532-3p表达明显上调，转染miR-532-3p-inhibitor的ESCs中miR-532-3p表达明显下调(P<0.05)。CCK-8及Transwell实验结果显示，转染miR-532-3p-mimic的ESCs增殖、侵袭能力明显减弱，转染miR-532-3p-inhibitor的ESCs增殖、侵袭能力明显增强(P<0.05)。Starbase网站及双荧光素酶实验发现，miR-532-3p与AKT3具有靶向关系，且miR-532-3p可调控AKT3的表达。结论 EM组织中miR-532-3p表达下调，上调miR-532-3p的表达可抑制ESCs的增殖和侵袭，降低AKT3的表达。miR-532-3p可能通过靶向调控AKT3的表达抑制ESCs增殖和侵袭，从而抑制EM的发展。更多还原

【Abstract】 Objective To investigate the expression of miR-532-3 p in endometriosis(EM) tissues and its effect mechanism on proliferation, invasion and AKT3 expression of endometriosis stromal cells(ESCs). Methods The ectopic endometrial tissues of 10 EM patients who underwent laparoscopy and curettage in Langfang People′s Hospital from November 2019 to March 2020 and normal endometrial tissues of 10 non-EM patients were selected as the research objects. ESCs were isolated from ectopic endometrial tissues of EM patients and normal endometrial stromal cells(NESCs) were isolated from normal endometrial tissues of non-EM patients. ESCs were transfected with miR-532-3 p-mimic, miR-532-3 p-inhibitor and the corresponding negative control, respectively. Cell proliferation and invasion were measured by cell counting kit-8(CCK-8) assay and Transwell assay. The relative expression levels of miR-532-3 p and AKT3 were detected by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR). The expression of AKT3 was detected by Western blot. The relationship between miR-532-3 p and AKT3 was detected by luciferase reporter gene. Results The results of qRT-PCR showed that the expression of miR-532-3 p in ectopic endometrial tissue and ESCs was down-regulated compared with normal endometrial tissue and NESCs(P<0.05). The expression of miR-532-3 p in ESCs was significantly up-regulated after miR-532-3 p-mimic was transfected, and the expression of miR-532-3 p was significantly down-regulated in ESCs after miR-532-3 p-inhibitor was transfected(P<0.05). The results of CCK-8 and Transwell assay showed that the proliferation and invasion ability of ESCs transfected with miR-532-3 p-mimic was significantly reduced, and the proliferation and invasion ability of ESCs transfected with miR-532-3 p-inhibitor was significantly enhanced(P<0.05). Starbase website and dual luciferase assay found that miR-532-3 p had a targeting relationship with AKT3 and miR-532-3 p could regulate AKT3 expression.Conclusions The expression of miR-532-3 p is down-regulated in EM. Up-regulating the expression of miR-532-3 p can inhibit the proliferation and invasion of ESCs, and reduce the expression of AKT3. MiR-532-3 p can inhibit the proliferation and invasion of ESCs by targeting the expression of AKT3, thereby inhibiting the development of EM.更多还原