miR‑132 is upregulated in polycystic ovarian syndrome and inhibits granulosa cells viability by targeting Foxa1.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic disorders characterized by hyperandrogenism, polycystic ovaries and ovulatory dysfunction. Several studies have suggested that the aberrant expression of microRNAs (miRNAs/miRs) plays an important role in the pathogenesis of PCOS; however, the role and underlying mechanisms of miR‑132 in the development of PCOS remain unclear. In the present study, the expression of miR‑132 in granulosa cells (GCs) derived from 26 patients with PCOS and 30 healthy controls was detected by reverse transcription-quantitative PCR (RT-qPCR). The apoptosis of GCs was examined using a TUNEL assay. The human ovarian granulosa-like tumor cell line, KGN, was cultured for Cell Counting Kit-8 assays following the overexpression or knockdown of miR‑132. TargetScan was applied to identify the potential targets of miR‑132, which was further verified by a luciferase assay, RT‑qPCR and western blotting. The expression of miR‑132 was decreased in GCs from patients with PCOS. Moreover, the GCs of patients with PCOS exhibited significantly increased apoptotic nuclei. Furthermore, the overexpression of miR‑132 inhibited the viability of KGN cells. In addition, the results verified that miR‑132 directly targeted forkhead box protein A1 (Foxa1), the knockdown of which suppressed KGN cell viability. On the whole, the findings of the present study demonstrated that miR‑132 inhibited cell viability and induced apoptosis by directly interacting with Foxa1. Thus, miR‑132 may be a potential target for the treatment of patients with PCOS. [ABSTRACT FROM AUTHOR]