The present study aimed to investigate the role and mechanisms of microRNA (miR)-33b in endometriosis (Ems). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), MTT assays, flow cytometry, caspase-3/9 activity assays and… Click to show full abstract
The present study aimed to investigate the role and mechanisms of microRNA (miR)-33b in endometriosis (Ems). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), MTT assays, flow cytometry, caspase-3/9 activity assays and western blotting were performed in the present study. Initially, miR-33b expression in an Ems rat model was investigated by RT-qPCR and was demonstrated to be upregulated in Ems tissue samples of rats compared with the control group. In addition, miR-33b upregulation inhibited cell growth and enhanced apoptosis in an Ems model (primary cell cultures) compared with the control group. In addition, miR-33b up-regulation reduced Wnt/β-catenin signaling pathway and suppressed zinc finger E-box-binding homeobox 1 (ZEB1) protein expression in the in vitro Ems model (primary cell cultures) compared with the control group. Furthermore, small interfering-ZEB1 ameliorated the effects of miR-33b downregulation on Ems cell growth in the in vitro Ems model. Additionally, a Wnt agonist reduced the effects of miR-33b upregulation on Ems cell growth in the in vitro Ems model. In conclusion, the present study demonstrated that upregulation of miR-33b may promote Ems through Wnt/β-catenin by ZEB1 expression.
               
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