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Erschienen in:
11.03.2022 | General Gynecology
MiR-518c-3p alleviates endometriosis by inhibiting ectopic endometrial migration and epithelial–mesenchymal transition via targeting ZNF608
Erschienen in: Archives of Gynecology and Obstetrics | Ausgabe 1/2023
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Purpose
The present study was performed to clarify the regulatory mechanism of miR-518c-3p in the progression of endometriosis (EMs).
Methods
MicroRNAs (miRNAs) potentially acting on EMs were predicted by bioinformatics databases and validated in normal and ectopic endometrium. The miR-518c-3p mimics were transfected into endometrial stromal cells (ESCs), and cell growth, death, and proliferation marker proteins expression were detected. The targeting relationship of miR-518c-3p with zinc finger protein 608 (ZNF608) was validated by luciferase reporter assay. ESCs were incubated with miR-518c-3p mimics alone or co-transfected with pcDNA-ZNF608, and growth, death, as well as proliferation and epithelial–mesenchymal transition (EMT) marker protein expression were detected. A rat model of EMs overexpressing miR-518c-3p alone or ZNF608 simultaneously was constructed to detect ectopic endometrial cell apoptosis and cyst volume in rats.
Results
MiR-518c-3p expression was downregulated in ectopic endometrium. MiR-518c-3p mimic inhibited migration, invasion and proliferation of ESCs, and promoted apoptosis. MiR-518c-3p targeted the 3'UTR of ZNF608. ZNF608 expression was upregulated in ESCs and ectopic endometrium, and the regulatory effect of pcDNA-ZNF608 on ESCs was opposite to that of miR-518c-3p mimics. ZNF608 overexpressing rats had greater endometrial cyst weight and volume, and decreased endometrial apoptosis compared with miR-518c-3p overexpressing alone.
Conclusion
MiR-518c-3p inhibited growth, metastasis and EMT of ESCs and decreased ectopic endometrial area in rats with EMs by targeting ZNF608.