ArticleArchives of medical science : AMS2022
The UCA1 and microRNA-18a signaling pathway mediates the irisin-lowering effect of metformin in the management of polycystic ovary syndrome.
Article in Archives of medical science : AMS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Non-coding molecular determinants of polycystic ovary syndrome: A future treatment potential.Journal of assisted reproduction and genetics · 2025Review
- miR-584-5p Regulates MSMO1 to Modulate the AKT/PI3K Pathway and Inhibit Breast Cancer Progression.Protein and peptide letters · 2025Article
- Evaluating the Efficacy of Irisin Injection in Mimicking the Molecular Responses Induced by Endurance Exercise in Mouse Liver Tissue.International journal of preventive medicine · 2024Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The present study aimed to clarify the underlying mechanism of metformin (met) in the management of polycystic ovary syndrome (PCOS) and to explore the role of the UCA1/microRNA-18a signaling pathway in the control of PCOS. Material and methods: Real-time PCR was performed to compare the levels of irisin, blood glucose, UCA1 and miR-18a among PCOS, PCOS + Met, and control groups using area under curve (AUC) values. In-silicon analysis and luciferase assay were performed to explore the regulatory relationship among UCA1, miR-18a and irisin. Real-time PCR and Western blot analysis were carried out to detect the effect of met on the expression of UCA1, miR-18a and irisin. Results: AUC of UCA1 was the highest while AUC of irisin was the lowest. Also, irisin and UCA1 levels in the PCOS group were much higher than those in the PCOS + Met group, while miR-18a level in the PCOS group was much lower than in the PCOS + Met group. Through the luciferase assay, miR-18a was proved to directly bind to the irisin 3'UTR. Additionally, irisin was identified to be a target gene of miR-18a. Finally, treatment with met at an increasing concentration reduced the level of UCA1 and irisin but increased the level of miR-18a in a dose-dependent manner. Conclusions: In the management of PCOS, the irisin-lowering effect of met is regulated by the UCA1/miR-18a/RhoB signaling pathway.
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