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目的 探讨卵巢子宫内膜异位症(EMs)是否发生了上皮-间质转化(EMT)现象,以及miR-200a在EMs中的表达情况及与EMT的关系,从分子水平上进一步阐明EMs侵袭转移的机制.方法 选取2017年1月—12月在苏州大学附属第一医院妇科因EMs和单纯卵巢囊肿行腹腔镜手术的患者各80 例.留取EMs患者的宫腔内膜组织和异位内膜组织以及单纯卵巢囊肿患者的宫腔正常内膜组织.提取各组织中的RNA和蛋白,采用RT-PCR方法检测miR-200a在各组织中的表达情况.采用Western blot方法检测EMT相关蛋白ZEB1和E-cadherin蛋白在各组织中的表达情况.结果 在不同内膜组织中,miR-200a有不同程度的表达.与正常子宫内膜组织相比,异位内膜和在位内膜中的表达水平明显降低,且异位内膜中表达水平较在位内膜组织下调.在不同内膜组织中,ZEB1、E-cadherin均有不同程度的表达.与正常内膜组织相比,异位内膜和在位内膜中的E-cadherin表达水平明显降低,且异位内膜组织E-cadherin表达水平明显低于在位内膜.相反,与正常内膜组织相比,异位内膜和在位内膜中ZEB1表达量明显升高,且异位内膜组织中的表达水平明显高于在位内膜组织.miR-200a的表达量与其对应组织中的E-cadherin的表达呈显著的正相关,与ZEB1的表达量呈显著的负相关.结论 卵巢EMs患者的异位及在位内膜中miR-200a表达降低,下调的miR-200a可能通过降低对EMT转录因子ZEB1的抑制作用从而促进ZEB1的表达,进而导致E-cadherin蛋白表达的减少,从而促使在位内膜组织发生了EMT,增加了妇女EMs的发病风险.“,”Objective To explore whether epithelial-mesenchymal transition (EMT) involved in the growth of endometrium outside the uterus, to analyze the expression of miR-200a in ovarian endometriosis and the relationship with EMT and consequently, to offer a theoretical foundation in molecular level for revealing the mechanisms of invasion and metastasis in endometriosis. Methods 80 patients with endometriosis and 80 patients with benign ovary cysts underwent laparoscopic surgery in the First Affiliated Hospital of Soochow University from January to December 2017 were selected. Eutopic and ectopic endometrium of patients with endometriosis and normal endometrium of patients with benign ovarian cysts were obtained. RNA and protein in each tissue were extracted, and the expression of miR-200a in each tissue was detected by RT-PCR. Western blot was used to detect the expression of EMT related proteins: ZEB1 and E-cadherin in each endometrium tissues. Results MiR-200a in each tissue had different degree expression. Compared with normal endometrium tissue, the expression level of miR-200a in ectopic and eutopic endometrium decreased obviously, and it was significantly lower in ectopic endometrium than in eutopic endometrium. ZEB1 and E-cadherin in each tissue had different degree expression. Compared with normal endometrium tissue, the expression level of E-cadherin in ectopic and eutopic endometrium decreased obviously, and it was significantly lower in ectopic endometrium than in eutopic endometrium. On the contrary, the expression level of ZEB1 in ectopic and eutopic endometrium increased significantly, and it was significantly higher in ectopic endometrium than in eutopic endometrium. The expression level of miR-200a had a significantly positive correlation with E-cadherin in corresponding tissues, meanwhile, miR-200a had a significantly negative correlation with ZEB1. Conclusion The expression of miR-200a in ectopic and eutopic endometrium of patients with ovarian endometriosis is decreased. The down-regulated miR-200a may promote the expression of ZEB1 by reducing the inhibition of EMT transcription factor ZEB1, thus leading to the decrease of the expression of E-cadherin protein, which promotes EMT in eutopic endometrium and increases the risk of endometriosis in women.