Aberrant expression of miR1271-5p in polycystic ovary syndrome and its regulatory effect on granulosa cells via targeting PRKAR1A.

INTRODUCTION

Polycystic ovary syndrome (PCOS) is characterized by ovulation disturbance, hyperandrogenemia, and polycystic ovary, causing infertility. There is a lack of unified conclusions on the pathogenesis of PCOS, resulting in challenges in the clinical management. This study evaluated the potential of miR-1271-5p in diagnosing PCOS and its regulatory effect on granulosa cells, aiming to explore a potential therapeutic target for PCOS.

MATERIAL AND

METHODS

This study enrolled 189 PCOS patients with 107 healthy women as the control group. Serum miR-1271-5p was assessed by quantitative polymerase chain reaction (qPCR), and its clinical significance was evaluated from the perspectives of diagnosis and correlation with clinical symptoms. In vitro, the regulatory effects of miR-1271-5p on granulosa cell injury (KGN cell induced by lipopolysaccharide, LPS) were evaluated from the perspectives of cell growth, apoptosis, oxidative stress, and inflammation. The regulatory mechanism was estimated through the target prediction.

RESULTS

miR-1271-5p was upregulated in PCOS, discriminating PCOS patients and correlated with obesity, insulin resistance, and hormone disturbance of PCOS patients. miR-1271-5p, and insulin resistance- and hormone-related features, was identified as risk factors for PCOS. In KGN cells, miR-1271-5p targeted PRKAR1A and negatively regulated its expression. Silencing miR-1271-5p could alleviate LPS-induced cell injury, including reduced cell viability, oxidative stress, and inflammation. Knocking down PRKAR1A could reverse the protective effects of miR-1271-5p on KGN cells.

CONCLUSIONS

miR-1271-5p served as a biomarker for PCOS, predicting disease risk and diagnosing disease onset. The miR-1271-5p/PRKAR1A axis regulated granulosa cell injury under LPS, which can be considered a potential therapeutic target for PCOS.