MiR-30c-5p targets SIRT1 to promote apoptosis in ovarian granulosa cells

Background : Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by abnormal follicular development and is the leading cause of infertility among women of reproductive age. miR-30c-5p, a newly discovered microRNA (miRNA), plays a crucial role in numerous pathological conditions, such as malignancies, reproductive dysfunctions, and metabolic irregularities. However, the role of miR-30c-5p in PCOS and the apoptosis of granulosa cells (GCs) is not fully understood. Research methods : GCs were isolated from the follicular fluid of 23 patients with PCOS and 21 normal controls. The expression of miR-30c-5p and Sirtuin 1 (SIRT1) was detected using quantitative real-time polymerase chain reaction (qRT-PCR). A Spearman correlation analysis was conducted to evaluate the relationship between the expression levels of these markers. Proliferation and apoptosis in human granulosa tumor cell lines (KGN) were analyzed following the overexpression or underexpression of miR-30c-5p, utilizing the Cell Counting Kit-8, flow cytometry, and western blot techniques. TargetScan was used to identify potential targets of miR-30c-5p, which were subsequently validated through qRT-PCR, western blot, and a dual luciferase reporter gene assay. Results : The results of our study suggest that the levels of miR-30c-5p aresignificantly elevated in individuals with PCOS compared with the control group. Conversely, we observed a significant decrease in the expression of SIRT1 in patients with PCOS compared with the control group. Moreover, miR-30c-5p expression was negatively correlated with SIRT1. The upregulation of miR-30c-5p suppressed the expression of SIRT1 and Bcl-2, inhibited GC proliferation, and increased the expression of Bax. Conclusion: Our findings suggest that miR-30c-5p inhibits the proliferation of KGN cells by targeting SIRT1. Thus, this study enhances the current understanding of the mechanisms underlying apoptosis in PCOS and GCs.