Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. miR-93-5p has been reported to be elevated in granulosa cells of PCOS patients. However, the mechanism by which miR-93-5p drives granulosa cell (GC) progression remains unclear. Thus, this study focuses on the roles and mechanisms of miR-93-5p in the GCs of PCOS.MethodsKGN cells have similar ovarian physiological characteristics and are used to study the function and regulatory mechanism of GCs. In this study, KGN cells were transfected with si-NC, si-miR93-5p, oe-NC and oe-miR93-5p. A cell counting kit-8 assay, flow cytometry and western blotting were performed to observe the proliferation and apoptosis of KGN in different groups. Subsequently, the levels of reactive oxygen species, malondialdehyde, GPX4, SLC7A11 and Nrf2, which are indicators of ferroptosis, were measured by a dihydroethidium fluorescent dye probe, biochemical kit, western blotting and reverse transcription quantitative polymerase chain reaction. Ultimately, bioinformatic analysis and experimental methods were used to examine the interaction between miR-93-5p and the NF-κB signaling pathway.ResultsmiR-93-5p was upregulated in the GCs of PCOS patients. Overexpression of miR-93-5p promoted apoptosis and ferroptosis in KGN cells, while knockdown of miR-93-5p showed the reverse effect. Biological analysis and subsequent experiments demonstrated that miR-93-5p negatively regulates the NF- κB signaling pathway.ConclusionmiR-93-5p promotes the apoptosis and ferroptosis in GC by regulating the NF-κB signaling pathway. Silencing of miR-93-5p protects against GC dysfunction. Our study identified miR-93-5p as a new molecular target for improving the function of GCs in PCOS patients.

Polycystic ovarian syndrome (PCOS) is the most common multifactor heterogeneous endocrine and metabolic disease in women of childbearing age. PCOS is a group of clinical syndromes characterized by reproductive disorders, metabolic disorders, and mental health problems that seriously impact the physical and mental health of patients. At present, new studies suggest that human evolution leads to the body changes and the surrounding environment mismatch adaptation, but the understanding of the disease is still insufficient, the pathogenesis is still unclear. Sirtuin 1 (SIRT1), a member of the Sirtuin family, is expressed in various cells and plays a crucial role in cell energy conversion and physiological metabolism. Pathophysiological processes such as cell proliferation and apoptosis, autophagy, metabolism, inflammation, antioxidant stress and insulin resistance play a crucial role. Moreover, SIRT1 participates in the pathophysiological processes of oxidative stress, autophagy, ovulation disturbance and insulin resistance, which may be a vital link in the occurrence of PCOS. Hence, the study of the role of SIRT1 in the pathogenesis of PCOS and related complications will contribute to a more thorough understanding of the pathogenesis of PCOS and supply a basis for the treatment of patients.

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