SnoRNA ENST00000391318 Suppressed Endometrial Receptivity by Competitively Binding To miRNA-3928-5p To Regulate CDH11 in Women in a GnRH Antagonist Stimulation Protocol

Abstract Background To determine the small nucleolar RNA (snoRNA) expression profiles in the endometrium during the implantation phase and identify their potential biological functions. Methods We used RNA sequencing to analyze the expression changes of snoRNAs in the endometrium of women during the implantation phase of the natural cycle and in the GnRH antagonist stimulation protocol. The expression of snoRNA ENST00000391318 was manipulated in endometrial cells by lentivirus. CCK-8, clone formation, flow cytometry, scratch and Transwell assays were used to detect the effects of ENST00000391318 on the proliferation, apoptosis, migration and invasion of endometrial cells. RNA pulldown and luciferase reporter gene experiments were used to detect the binding of ENST00000391318 to miRNA. Results Endometrial SNORNA ENST00000391318 was upregulated in the GnRH antagonist stimulation protocol. SNORNA ENST00000391318 overexpression inhibited cell proliferation and the cell cycle in Ishikawa cells, and SNORNA ENST00000391318 knockdown promoted cell proliferation and the cell cycle in Ishikawa cells. SNORNA ENST00000391318 overexpression inhibited cell migration and invasion in Ishikawa cells. SNORNA ENST00000391318 inhibited the expression of endometrium receptivity factor. miRNA-3928-5p is a target of SNORNA ENST00000391318 in Ishikawa cells. SNORNA ENST00000391318 regulates the expression of CDH11 through interaction with miRNA-3928-5p in Ishikawa cells. Conclusions The ENST00000391318/miR-3928-5p/CDH11 signaling pathway can regulate the receptivity of the endometrium for patients in the GnRH antagonist stimulation protocol. SNORNA ENST00000391318 downregulates the function of miR-3928-5p through a ceRNA mechanism to upregulate the expression of CDH11. SNORNA ENST00000391318 downregulates the receptivity of the endometrium by upregulating the expression of CDH11.