Role of miR‑139‑5p in ectopic endometrial stromal cells and the underlying molecular mechanism

Endometriosis is an estrogen‑dependent disease. Studies have shown that miR‑139‑5p significantly upregulated in endometriosis lesions, but its specific role and molecule mechanism has not yet been reported. The malignant biological behavior of ectopic endometrial stromal cells (ESCs) similar to cancer cells. BBC3 (BCL2 binding component 3) a known apoptosis inducer it serves key roles the regulation cell behavior. However, ESCs remains unknown. present study aimed investigate progression determine underlying molecular action. Ectopic, non‑ectopic normal were extracted from samples, reverse transcription‑quantitative PCR was performed microRNA (miR)‑139‑5p Bcl‑2 3 (BBC3) mRNA expression levels tissue samples ESCs. target gene predicted using TargetScan software verified dual luciferase reporter assay. Western blotting protein levels. Flow cytometry analysis, MTT Transwell assays assess apoptosis, viability, migration invasion transfected with inhibitor control, inhibitor, + control‑small interfering (si)RNA or BBC3‑siRNA, respectively. results demonstrated compared respective control groups. Furthermore, direct miR‑139‑5p, both downregulated Both transfection BBC3‑small markedly ESCs, inhibitor‑induced reversed following BBC3‑siRNA. decreased invasion, while inducing group. Notably, aforementioned effects by knocking down expression. In conclusion, suggested may play regulating viability directly targeting BBC3.