MicroRNA-125b controls growth of ovarian granulosa cells in polycystic ovarian syndrome by modulating cyclin B1 expression

Introduction: There is a lot of evidence that suggests that microRNAs (miRs) play an imperative role in the pathogenesis of polycystic ovary syndrome (PCOS). This study was designed to decipher the role of miR-125b in PCOS pathogenesis. Material and methods: Expression analysis of miR-125b was determined by real-time quantitative polymerase chain reaction and the KGN ovarian granulosa cell viability was examined by CCK-8 assay. DAPI assay and flow cytometry were carried out for the detection of apoptosis and cell cycle distribution respectively. Protein levels were checked by immunoblotting. Results: The miR-125b transcript levels were considerably high in polycystic ovaries and ovarian granulosa KGN cells. The inhibition of miR-125b expression decreased the viability of the KGN cells by arresting the cells at the G2/M check point. Target Scan analysis revealed cyclin B1 as the target of miR-125b and suppression of miR-125b caused considerable up-regulation of cyclin B1 expression. Like miR-125b inhibition, cyclin B1 silencing also inhibited the KGN cell viability via G2/M arrest. Ectopic expression of miR125b was unable to nullify the effects of cyclin-B silencing on KGN cell viability but the overexpression of cyclin B1 nullified the effects of the miR-125b suppression on KGN cell proliferation. Conclusions: Since miR-125b controls the proliferation rate of granulosa cells in polycystic ovaries, it might be addressed as a potential therapeutic target for PCOS patients com

Automated summary

This study revealed the important role of miR-125b in the pathogenesis of PCOS, as it controls the proliferation rate of granulosa cells in polycystic ovaries. The inhibition of miR-125b decreased cell viability by regulating cyclin B1 expression, suggesting that miR-125b could be a potential therapeutic target for PCOS patients.