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Updated: Sep 30, 2025
A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
Published on: November 24, 2020
MiR-518c-3p alleviates endometriosis by inhibiting ectopic endometrial migration and epithelial-mesenchymal
Bin Lu1,2, Xiaohui Cao3, Xinhua Chen2
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow University, Yunxiu Building, No.1 Shizi Street, Canglang District, Suzhou, 215006, Jiangsu, China.
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.
Insights
MicroRNA-518c-3p inhibits endometriosis progression by targeting ZNF608. This microRNA (miRNA) reduces cell growth and metastasis, offering a potential therapeutic target for endometriosis.
Area of Science:
- Reproductive biology
- Molecular endocrinology
- Oncology
Background:
- Endometriosis (EMs) is a debilitating gynecological condition.
- MicroRNAs (miRNAs) play crucial roles in cellular processes relevant to EMs.
- Understanding miRNA regulation in EMs is vital for developing new therapies.
Purpose of the Study:
- To elucidate the regulatory mechanism of miR-518c-3p in endometriosis progression.
- To investigate the role of miR-518c-3p in endometrial stromal cells (ESCs) and an EMs rat model.
- To identify potential therapeutic targets for endometriosis.
Main Methods:
- Bioinformatic prediction and validation of miRNAs in normal and ectopic endometrium.
- In vitro studies using ESCs transfected with miR-518c-3p mimics and ZNF608.
- Luciferase reporter assay to confirm miR-518c-3p targeting of ZNF608.
- In vivo studies using a rat model of EMs.
Main Results:
- MiR-518c-3p expression was significantly downregulated in ectopic endometrium.
- MiR-518c-3p inhibited ESCs migration, invasion, proliferation, and promoted apoptosis.
- MiR-518c-3p directly targeted the 3' untranslated region (3'UTR) of ZNF608.
- ZNF608 overexpression reversed the inhibitory effects of miR-518c-3p in vitro and exacerbated EMs in vivo.
Conclusions:
- MiR-518c-3p acts as a tumor suppressor in endometriosis by inhibiting cell growth, metastasis, and epithelial-mesenchymal transition (EMT).
- The miR-518c-3p/ZNF608 axis is a critical regulatory pathway in endometriosis progression.
- Targeting miR-518c-3p or ZNF608 may offer novel therapeutic strategies for endometriosis.
