Case-control study demonstrates reduced serum miR-5584-5p in endometriosis, indicating its diagnostic value and function in suppressing cellular invasion via FZD2.
Key Points
To evaluate the diagnostic utility of serum miR-5584-5p in endometriosis and determine its functional role in disease progression through FZD2 targeting.
Enrolled 217 dysmenorrhea patients (107 endometriosis cases and 110 controls) in a case-control design.
Modulated miR-5584-5p and FZD2 in Ishikawa cells to evaluate cell proliferation, migration, invasion, dual-luciferase binding, and Wnt/β-catenin transcriptional activity.
Serum miR-5584-5p was significantly downregulated in endometriosis patients, yielding high diagnostic accuracy (AUC = 0.903) as an independent protective factor.
Overexpression of miR-5584-5p suppressed Ishikawa cell proliferation, migration, and invasion while inhibiting the epithelial-mesenchymal transition (EMT) and Wnt/β-catenin signaling.
FZD2 was identified as a direct target of miR-5584-5p, and restoring FZD2 expression reversed the suppressive effects of miR-5584-5p on aggressive cellular phenotypes.