Downregulated miR-363-5p causes recurrent spontaneous abortion (RSA) by regulating the S100A1 expression

Recurrent spontaneous abortion (RSA) involves complex pathophysiology, making it difficult to develop effective treatments and causing significant health and economic burdens. This study evaluated miR-363-5p as a potential biomarker for RSA and explored its role in disease progression to provide insights for clinical management.

A total of 68 serum samples from RSA patients and 97 from healthy pregnant controls were analyzed to determine miR-363-5p expression and its clinical significance. The EVT cell line HTR-8/SVneo was used for in vitro experiments. Cell proliferation was assessed using CCK-8 assays, while Transwell assays evaluated migration and invasion. qRT-PCR detected miR-363-5p and S100A1 expression levels. Dual-luciferase reporter assays confirmed the interaction between miR-363-5p and S100A1.

miR-363-5p expression was significantly lower in RSA patients than in healthy pregnant controls. ROC analysis indicated its high diagnostic potential for RSA. In vitro experiments showed that miR-363-5p promoted HTR-8/SVneo cell proliferation, migration, and invasion while inhibiting apoptosis. S100A1 was identified as a direct target of miR-363-5p in RSA. miR-363-5p regulates EVT cell functions by suppressing S100A1 expression.

Serum miR-363-5p downregulation may serve as a diagnostic biomarker for RSA. miR-363-5p likely affects pregnancy outcomes in RSA by targeting S100A1 to regulate EVT cell functions. These findings suggest that miR-363-5p has potential for both diagnosing and treating RSA.