Study On The Mechanism Of Long Chain Non-coding LncRNA110289 In Regulating Endometrial Receptivity In Patients With Endometriosis

[Background]Endometriosis(EM)is a common and difficult disease in women of childbearing age,and about 40%to 50%of the patients will have infertility symptoms,but the mechanism is not clear.Studies have suggested capacitive damage of the endometrium in patients.Receptivity refers to the state of biological processes in which the endometrium allows the embryo to adhere,invade and implant during the implantation window.Long non-coding RNA(lncRNA)has been shown to be involved in endometrial receptivity formation.However,there is currently a lack of relevant reports on lncRNA and endometrial receptivity formation in EM patients.[Objective]To explore the role of lncRNA110289 in endometrial receptivity impairment in EM patients,analyze the molecular mechanism of endometrial receptivity impairment in patients with endometriosis,and provide new ideas for improving the reproductive outcome of patients.[Methods]1.Clinical samples were collected and the expression levels of lncRNA110289,endometrial receptivity gene integrin subunit 3 ITGB3 and OPN were detected by fluorescence PCR in patients with non-ectopic pregnancy compared with those with ectopic infertility.2.Bioinformatics and in situ hybridization analysis of lncRNA localization and biochemical information,lncRNA expression profile,bioinformatics screening of miRNA molecules that lncRNA110289 may be regulated by ceRNA mechanism.3.CCK8 detected the difference in cell proliferation between the proliferative stage and the secretory stage,and transwell analyzed the migration capacity of decidualized cells.4.Overexpression of lncRNA110289.Blastocyst adhesion experiment verified the change of adhesion ability of endometrial cells after overexpression of lncRNA110289.[Results]The expression levels of lncRNA110289,ITGB3 and OPN were significantly decreased in endometriosis patients.LncRNA110289 was located in cytoplasm.After overexpression of LncRNA110289 in interstitial cells,the expression of ITGB3 and OPN could be promoted.The migration ability of mesenchymal cells was enhanced after decidualization,and the total number of cells in the proliferative stage was significantly higher than that in the secretory stage.Changes in adhesion of endometrial cells after overexpression of LncRNA110289.After progesterone treatment,the expression levels of lncRNA110289,ITGB3 and OPN increased significantly.Bioinformatics analysis showed that lncRNA110289,let-7 and ITGB3 had binding sites.Overexpression of LncRNA 110289 led to a decrease in let-7 of miRNA.[Conclusion]Abnormally low expression of lncRNA 110289 may lead to increased expression of endometrial receptivity genes ITGB3 and OPN by adsorption of let-7 by ceRNA mechanism,thus promoting the biological process of endometrial receptivity impairment in patients with endometriosis.