Differential expression of microRNA-3127-5p and its molecular mechanisms in polycystic ovary syndrome.

Introduction: The present study was undertaken to elucidate the expression status and molecular mechanism underlying microRNA-3127-5p (miR-3127-5p) in polycystic ovary syndrome (PCOS).

Material And Methods: A total of 50 PCOS and 50 non-PCOS patients were recruited as research subjects. Quantitative real-time polymerase chain reaction was employed to assess the relative abundances of miR-3127-5p in serum, cumulus cells (CCs), and granulosa cells (GCs) from PCOS patients. Additionally, cellular activities and ferroptosis-related biomarkers were evaluated. Bioinformatics analysis was conducted to identify potential targets of miR-3127-5p. To validate the interaction between miR-3127-5p and sorbin and SH3 domain-containing protein 1 (SORBS1), a luciferase reporter assay was conducted.

Results: Enforced miR-3127-5p expression was detected in serum, CCs, and GCs from PCOS patients, demonstrating a robust diagnostic capacity for effectively distinguishing between PCOS and non-PCOS patients. Furthermore, the reduction of miR-3127-5p expression was found to enhance cell viability and inhibit cell apoptosis in human granulosa-like tumor cell line (KGN) and the luteinized granulosa cell line (SVOG) cells. Concurrently, its down-regulation led to attenuated levels of iron, malondialdehyde (MDA), and reactive oxygen species (ROS), while simultaneously increasing the expression of glutathione peroxidase 4 (GPX4). Notably, miR-3127-5p expression exhibited an inverse relationship with SORBS1. Rescue experiments revealed that the effects of downregulated miR-3127-5p expression on cellular behaviors and ferroptosis were reserved through the transfection of si-SORBS1.

Conclusion: The downregulation of miR-3127-5p expression facilitates cell growth and attenuates ferroptosis by targeting SORBS1, thereby playing a pivotal role in the initiation and development of PCOS.