miR-323-3p regulates the steroidogenesis and cell apoptosis in polycystic ovary syndrome (PCOS) by targeting IGF-1.

Polycystic ovary syndrome (PCOS) is an endocrine and metabolic heterogeneous disorder. The incidence of which reaches 5% to 10% among reproductive-age women. Abnormal folliculogenesis is considered to be a common characteristic of PCOS, but the cause of this disorder and its pathogenesis still remain uncertain. Previous studies had proved that dysregulation of microRNAs is related to the pathogenesis of PCOS. In this study, we investigated the effect of miR-323-3p on the human cumulus cells (CCs). We also investigated the underlying mechanisms of miR-323-3p on human granulosa-like tumor cell line (KGN) or primary human CCs by stimulating with Dihydrotestosterone (DHT). Our findings suggested that the level of miR-323-3p in human CCs of women with PCOS was down-regulated, compared with that of the control group. Moreover, the inhibition of the level of miR-323-3p could up-regulate of the steroidogenesis and promote the apoptosis in KGN cells. In addition, our data confirmed that the Insulin-like growth factor 1 (IGF-1) gene was the direct target of miR-323-3p. Furthermore, the mimic of miR-323-3p inhibited the expression of IGF-1, which down-regulated the levels of AR, AMHR-II, CYP19A, EGFR, and GATA-4. In conclusion, miR-323-3p targeting IGF-1 regulates the steroidogenesis and the activity of CCs, which plays an important role in the occurrence and development of PCOS. Our results have shown that miR-323-3p is a novel and promising molecular target for the improvement of the dysfunction of CCs in PCOS.