MicroRNA-125b controls growth of ovarian granulosa cells in polycystic ovarian syndrome by modulating cyclin B1 expression
Related Experiment Video
Updated: Sep 22, 2025

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Jie Deng1, Chanyu Li1, Jianbo Luo1
1Department of Gynecology, the First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
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 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.
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.
Insights
MicroRNAs (miRs) are implicated in polycystic ovary syndrome (PCOS). This study found that miR-125b is highly expressed in PCOS ovaries and regulates granulosa cell proliferation by targeting cyclin B1, suggesting miR-125b as a potential therapeutic target for PCOS.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRs) are increasingly recognized for their role in the pathogenesis of polycystic ovary syndrome (PCOS).
- Understanding the specific functions of individual miRs in PCOS is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of miR-125b in the pathogenesis of polycystic ovary syndrome (PCOS).
- To elucidate the molecular mechanisms by which miR-125b influences ovarian granulosa cell function in PCOS.
Main Methods:
- Quantitative real-time PCR for miR-125b expression analysis.
- Cell viability assays (CCK-8), apoptosis detection (DAPI), and cell cycle analysis (flow cytometry) in KGN cells.
- Protein expression analysis using immunoblotting and TargetScan for predicting miR-125b targets.
Main Results:
- miR-125b transcript levels were significantly elevated in polycystic ovaries and KGN granulosa cells.
- Inhibition of miR-125b reduced KGN cell viability by inducing G2/M cell cycle arrest.
- Cyclin B1 was identified as a direct target of miR-125b; its suppression mimicked miR-125b inhibition effects, while its overexpression counteracted miR-125b suppression effects.
Conclusions:
- miR-125b plays a significant role in controlling the proliferation of granulosa cells in the context of PCOS.
- The findings suggest that miR-125b, through its regulation of cyclin B1, is a potential therapeutic target for PCOS management.
More Related Videos
Related Concept Videos
Hormonal Control of the Ovarian Cycle
Before puberty, the hypothalamus releases GnRH in a low frequency, low amplitude pulsatile manner. This along with the immature hypothalamic-pituitary-gonadal axis activity, results in low estrogen levels and the absence of a fully functional ovarian cycle. At puberty, GnRH secretion increases in both frequency and...
MicroRNAs
Hormonal Regulation of the Menstrual Cycle
At puberty, GnRH begins a pulsatile release pattern, which triggers the anterior pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The frequency and amplitude of GnRH pulses vary across the menstrual cycle, with faster pulses favoring LH release and slower pulses favoring FSH...
Folliculogenesis
Ovarian Cycle

