Diagnostic and mechanistic roles of miR-5584-5p in endometriosis via the FZD2-mediated Wnt/β-catenin EMT axis

Background The early detection of endometriosis (EM), a significant cause of dysmenorrhea, is essential for effective clinical management. This study sought to determine the functional role of miR-5584-5p in EM and the mechanistic involvement of its target, FZD2, in disease progression.

This case-control study enrolled 217 dysmenorrhea patients (107 EM cases and 110 controls). Ishikawa cells with modulated miR-5584-5p and FZD2 expression were used to assess cell proliferation, migration, and invasion. The miR-5584-5p/FZD2 interaction and Wnt/β-catenin transcriptional activity were validated by dual-luciferase and TOP/FOP flash reporter assays.

Serum miR-5584-5p was significantly downregulated in EM patients, demonstrating high diagnostic accuracy (AUC = 0.903) and acting as an independent protective factor. In vitro, miR-5584-5p overexpression suppressed Ishikawa cell proliferation, migration, and invasion, concurrently inhibiting Wnt/β-catenin transcriptional activity and the epithelial-mesenchymal transition (EMT) axis. FZD2 was confirmed as a direct target of miR-5584-5p. Crucially, FZD2 overexpression partially reversed the inhibitory effects of miR-5584-5p on malignant cellular phenotypes and restored Wnt/β-catenin signaling.

Serum miR-5584-5p serves as a valuable potential diagnostic biomarker for EM. Functionally, it attenuates endometrial epithelial cell aggressiveness by targeting FZD2 and suppressing the Wnt/β-catenin-EMT axis. Future studies utilizing primary cells and in vivo models are warranted to validate these preliminary mechanisms.

Not applicable. Funding No funding was received to assist with the preparation of this work. Author information Authors and Affiliations Corresponding author Ethics declarations Ethics approval and consent to participate The study received approval from the Ethics Committee of Guangdong Corps Hospital of People’s Armed Police and adhered to the ethical principles of the Declaration of Helsinki. Written informed consent was obtained from all participants. Consent for publication Not applicable. Competing interests The authors declare no competing interests. Additional information Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. About this article Cite this article Zhang, W., Zhang, M., Lu, H. et al. Diagnostic and mechanistic roles of miR-5584-5p in endometriosis via the FZD2-mediated Wnt/β-catenin EMT axis. Hereditas (2026). https://doi.org/10.1186/s41065-026-00732-4 Received: Accepted: Published: DOI: https://doi.org/10.1186/s41065-026-00732-4