Background
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disease in women at childbearing age. Several circular RNAs (circRNAs) have been demonstrated to be involved in PCOS. In this study, we aimed to explore the function and mechanism of circ_0043532 in PCOS.
Conclusion
Deficiency of circ_0043532 suppressed cell proliferation and induced cell cycle arrest and cell apoptosis in PCOS by modulation of miR-182/SGK3 axis.
Methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the expression of circ_0043532, miR-182 and serum/glucocorticoid regulated kinase family member 3 (SGK3). Cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine (EdU) assay and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Flow cytometry analysis was employed to evaluate cell cycle and cell apoptosis. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were conducted to verify the association between miR-182 and SGK3. Western blot assay was carried out to determine the protein level of SGK3.
Results
Circ_0043532 was markedly elevated in PCOS granulosa cells (GCs) and KGN cells. Silencing of circ_0043532 suppressed cell proliferation and cell cycle process and promoted cell apoptosis in PCOS GCs and KGN cells. For mechanistic analysis, circ_0043532 was identified as a sponge of miR-182 and SGK3 was confirmed to be a target gene of miR-182. Inhibition of miR-182 rescued the impacts of circ_0043532 interference on PCOS GCs and KGN cell progression. Moreover, miR-182 overexpression suppressed cell proliferation and cell cycle process and promoted cell apoptosis in PCOS GCs and KGN cells by targeting SGK3.