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Updated: Feb 17, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
miR-30c may serve a role in endometriosis by targeting plasminogen activator inhibitor-1
Xiaoli Chen1, Yan Jiang2, Dianling Pan3
1Department of Reproductive Medicine, Affiliated Hospital of Jining Medical University, Jining, Shandong 272000, P.R. China.
Abstract:
The present study aimed to investigate the role of miR-30c in endometriosis (EMs) and the underlying mechanism. The expression of miR-30c and plasminogen activator inhibitor type 1 (PAI-1) mRNA in EMs tissues was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and the expression of PAI-1 protein was detected by western blot analysis. The proliferation, migration, invasion and adhesion of endometrial stromal cells (ESCs) in different groups transfected with miR-30c mimic or inhibitor were compared. It was demonstrated that miR-30c expression in ectopic and eutopic endometriosis tissues were significantly lower than in normal endometrial tissue. However, PAI-1 mRNA expression in ectopic and eutopic endometrial tissues was higher than in normal endometrial tissues. Furthermore, the expression of PAI-1 protein was higher in ectopic and eutopic endometrosis tissues than in normal tissues. RT-qPCR results indicated that miR-30c expression was significantly increased or decreased in ESCs following transfection of mimic or inhibitor of miR-30c, respectively. Overexpression of miR-30c repressed the expression of PAI-1 mRNA and protein, while inhibition of miR-30c upregulated the expression of PAI-1 in ESCs. In addition, the invasion, migration, proliferation and adhesion of ESCs was repressed following the overexpression of miR-30c, whereas they were promoted when miR-30c expression was downregulated. The results of the present study indicated that miR-30c serves an important role in the development and progression of EMs by regulating the expression of PAI-1.
Insights
MicroRNA-30c (miR-30c) is downregulated in endometriosis, a condition affecting endometrial stromal cells. Its regulation of plasminogen activator inhibitor-1 (PAI-1) impacts disease progression.
Area of Science:
- Molecular Biology
- Gynecology
- Cell Biology
Background:
- Endometriosis (EMs) is a complex gynecological condition characterized by the presence of endometrial tissue outside the uterus.
- The molecular mechanisms underlying endometriosis progression, including cellular proliferation, migration, invasion, and adhesion, require further elucidation.
- MicroRNAs (miRNAs) are emerging as critical regulators in various biological processes and diseases, including endometriosis.
Purpose of the Study:
- To investigate the role of microRNA-30c (miR-30c) in the pathogenesis of endometriosis.
- To elucidate the underlying molecular mechanism by which miR-30c influences endometriosis progression.
- To examine the relationship between miR-30c and plasminogen activator inhibitor-1 (PAI-1) in endometrial stromal cells (ESCs).
Main Methods:
- Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect miR-30c and PAI-1 mRNA expression in endometriosis tissues and ESCs.
- Western blot analysis was employed to assess PAI-1 protein levels in tissue samples.
- In vitro experiments involved transfecting ESCs with miR-30c mimics or inhibitors to evaluate effects on cell proliferation, migration, invasion, and adhesion.
Main Results:
- miR-30c expression was significantly lower in ectopic and eutopic endometriosis tissues compared to normal endometrial tissue.
- Conversely, PAI-1 mRNA and protein expression were elevated in endometriosis tissues.
- Overexpression of miR-30c in ESCs repressed PAI-1 expression and inhibited cell proliferation, migration, invasion, and adhesion; conversely, inhibition of miR-30c promoted these processes.
Conclusions:
- miR-30c plays a crucial role in the development and progression of endometriosis.
- miR-30c exerts its effects by negatively regulating the expression of PAI-1.
- Targeting miR-30c may represent a potential therapeutic strategy for managing endometriosis.
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