miR-613 inhibits the proliferation of human ovarian granulosa cells by arresting cell cycle progression via the targeting of IGF-1

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder, and microRNA (miRNA) molecules have been implicated in the pathological process of PCOS. The aim of the present study was to elucidate the regulatory effects of miR-613 and insulin-like growth factor-1 (IGF-1) on the pathological process of polycystic ovary syndrome (PCOS). The targeting of IGF-1 by miR-613 was investigated by dual-luciferase reporter assay. The regulatory effect of miR-613 on the mRNA and protein levels of IGF1 was determined by reverse transcription-quantitative PCR and western blot analysis. The regulatory effects of miR-613 and IGF-1 on the proliferation and cell cycle progression of KGN cells were evaluated by colony formation assay and flow cytometric analysis. The results revealed that miR-613 targeted IGF-1 and reduced its translational level. In KGN cells, miR-613 arrested cell cycle progression in the G2/M phase and downregulated the expression of cyclin D1 and CDK1. The overexpression of IGF-1 attenuated the inhibitory effects of miR-613 on cell cycle arrest, cyclin D1 and CDK1 expression, and the proliferation of KGN cells. In conclusion, the present study demonstrated that miR-613 targets IGF-1 and thus suppresses its translation. It arrests cell cycle progression and attenuates the proliferation of KGN cells via the targeting of IGF-1. Therefore, it is suggested that miR-613 and IGF-1 could potentially be diagnostic biomarkers and therapeutic targets for PCOS.

Automated summary

This study demonstrated that miR-613 targets IGF-1 to suppress its translation, leading to cell cycle arrest and attenuated proliferation of KGN cells. This suggests that miR-613 and IGF-1 could serve as potential diagnostic biomarkers and therapeutic targets for PCOS.