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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
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Downregulated miR-363-5p causes recurrent spontaneous abortion (RSA) by regulating the S100A1 expression
Guimei Zhang1, Yingxuan Huang2,3, Lin Zheng4
1Department of Gynecology and Obstetrics, Anze Medical Group Traditional Chinese Medicine Hospital, Linfen, 042500, China.
Journal of Assisted Reproduction and Genetics
|November 10, 2025
Summary
Serum miR-363-5p is significantly lower in recurrent spontaneous abortion (RSA) patients. This microRNA may serve as a diagnostic biomarker and therapeutic target for RSA by regulating trophoblast cell function.
Area of Science:
- Reproductive biology
- Molecular diagnostics
- Biomarker discovery
Background:
- Recurrent spontaneous abortion (RSA) presents complex challenges in treatment and management.
- Identifying reliable biomarkers for RSA is crucial for early diagnosis and intervention.
Purpose of the Study:
- To evaluate miR-363-5p as a potential diagnostic biomarker for RSA.
- To investigate the role of miR-363-5p in the pathophysiology of RSA.
Main Methods:
- Serum samples from RSA patients (n=68) and healthy controls (n=97) were analyzed for miR-363-5p expression.
- In vitro studies used the HTR-8/SVneo cell line to assess cell proliferation, migration, invasion, and apoptosis.
- qRT-PCR and dual-luciferase reporter assays were employed to confirm molecular interactions.
Main Results:
- miR-363-5p expression was significantly downregulated in RSA patients compared to controls.
- miR-363-5p promoted trophoblast cell proliferation, migration, and invasion while inhibiting apoptosis.
- S100A1 was identified as a direct target of miR-363-5p, mediating its effects on trophoblast cell function.
Conclusions:
- Downregulated serum miR-363-5p shows potential as a diagnostic biomarker for RSA.
- miR-363-5p influences RSA by targeting S100A1 and regulating extravillous trophoblast (EVT) cell functions.
- miR-363-5p may offer a dual role in diagnosing and potentially treating RSA.
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