Inhibition of microRNA-19b promotes ovarian granulosa cell proliferation by targeting IGF-1 in polycystic ovary syndrome

The purpose of the present study was to investigate the functional role of microRNA (miR)-19b in polycystic ovary syndrome (PCOS) and try to elucidate its underlying mechanisms. Expression of miR‑19b and insulin‑like growth factor 1 (IGF-1) was examined in ovarian cortexes [(from 18 women with PCOS and 10 who did not have PCOS (non‑PCOS)] and KGN cells. Cell proliferation assays (cell viability and colony formation assay) were performed following overexpression or inhibition of miR‑19b and IGF‑1 or following insulin treatment in KGN cells. Expression levels of the cell cycle-associated protein cyclin D1 and cyclin‑dependent kinase (CDK) 1 were analyzed following overexpression or inhibition of miR-19b and IGF-1. Potential miR‑19b targets were identified by bioinformatics. Luciferase assay, reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to determine whether IGF‑1 was a target of miR‑19b. miR‑19b expression was significantly decreased in the PCOS ovarian cortex and KGN cells and its identified target, IGF‑1, was upregulated. miR‑19b overexpression inhibited cell proliferation at G2/M phrase. Overexpression of IGF‑1 promoted cell viability and colony formation ability in KGN cells. The expression of cyclin D1 and CDK1 was statistically increased by inhibition of miR‑19b and overexpression of IGF‑1. High concentrations of insulin decreased levels of miR‑19b, stimulated KGN cell proliferation, and elevated IGF‑1 levels. Inhibition of miR‑19b promoted ovarian granulosa cell proliferation by targeting IGF‑1 in PCOS. Insulin decreased the expression levels of miR‑19b and stimulated cell proliferation. The present study suggested that overexpression of miR‑19b may be a potential therapeutic approach for PCOS.