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Circular RNA ciR-02852: A novel physiological inhibitor of Porcine ovarian granulosa cell functions

Zuzana Fabová; Barbora Loncová; Abdel Halim Harrath; Anouar Feriani; Alexander V. Sirotkin
Molecular Biology Reports · Vol. 53, Issue 1 · 2026

Abstract

Background Circular RNAs (circRNAs) are stable epigenetic regulators of various biological processes, yet the functional role of ciR-02852 remains unknown. This study aimed to characterize the influence of ciR-02852 on the fundamental functions of porcine ovarian granulosa cells. Methods Cells were transfected with either a ciR-02852-overexpressing vector or an shRNA ciR-02852-knockdown vector. We assessed cell viability, proliferation markers (PCNA, cyclin B1), apoptosis markers (Bax, caspase-3, and DNA fragmentation), and the secretion of steroid (progesterone, testosterone, estradiol) and peptide (IGF-I, oxytocin) hormones via RT-qPCR, immunocytochemistry, TUNEL, and ELISA. Results Overexpression of ciR-02852 significantly reduced cell viability and the expression of PCNA and cyclin B1. Conversely, it stimulated both cytoplasmic and nuclear apoptosis, as evidenced by increased Bax, caspase-3, and DNA fragmentation. Furthermore, ciR-02852 overexpression inhibited the release of all measured hormones. Silencing of ciR-02852 via shRNA yielded the opposite effects, promoting proliferation and hormone output while suppressing apoptosis. Conclusion These findings demonstrate for the first time that ciR-02852 acts as a potent physiological inhibitor of porcine ovarian cell functions. Our results indicate that ciR-02852 could be a multi-target regulator of folliculogenesis and hormone production, highlighting its potential as a diagnostic marker or therapeutic target for managing reproductive disorders and improving animal production.

Bibliographic Information

JournalMolecular Biology Reports
PublisherSpringer
Publication Date2026-12-01
Publication Year2026
Volume53
Issue1
Document TypeJournal Article
Print ISSN0301-4851
eISSN1573-4978
DOI10.1007/s11033-026-11539-x

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NARA Access Coverage1973-01-01~Current
Journal Homepagehttps://www.springer.com/journal/11033
Publisher PageOpen Publisher Page
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