• Jie Deng, Chanyu Li, Jianbo Luo, Jiaqiong Xie, Cong Peng, and Xiaoyang Deng.
• Department of Gynecology, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
• Arch Med Sci. 2022 Jan 1; 18 (3): 746752746-752.

IntroductionThere 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 MethodsExpression 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.ResultsThe 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 miR-125b 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.ConclusionsSince miR-125b controls the proliferation rate of granulosa cells in polycystic ovaries, it might be addressed as a potential therapeutic target for PCOS patients.Copyright: © 2019 Termedia & Banach.

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