ArticleReproductive sciences (Thousand Oaks, Calif.)2026
Possible Involvement of miR-26a-3p in Regulating Cyclin D1(CCND1) in the Pathogenesis of Premature Ovarian Insufficiency (POI).
Article in Reproductive sciences (Thousand Oaks, Calif.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Premature ovarian insufficiency (POI) affects female fertility; however, the mechanisms are not yet fully understood. The aim of this study was to investigate the relationships among bisphenol A (BPA), microRNAs (miRNAs), and the cell cycle-related protein Cyclin D1 (CCND1) in ovarian granulosa cells. Using cell culture and transfection techniques, we analysed the effects of BPA on the proliferation of ovarian granulosa cells. Concurrently, qRT‒PCR and Western blotting were employed to assess miRNA expression levels and CCND1 protein levels, respectively. Our results demonstrated that BPA significantly inhibited the proliferation of ovarian granulosa cells. This inhibition was closely associated with the upregulation of specific miRNA expression and the downregulation of CCND1 protein expression. Furthermore, the overexpression of the identified miRNAs partially reversed the BPA-induced changes in CCND1 expression. These findings reveal a potential role for BPA in POI pathogenesis through the regulation of miRNAs and the cell cycle protein CCND1, providing a novel perspective on the mechanisms underlying this disorder. Future research should further elucidate the specific roles of these miRNAs and CCND1 in ovarian insufficiency and explore their potential application as therapeutic targets.
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