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

Lixia Feng, Xu Chen, Shenghua Zhang, Yunxia Chen, Yanling Yu
Experimental and therapeutic medicine · 2021 · vol. 22(5) , pp. 1251 · doi:10.3892/etm.2021.10686 · PMID:34539847 · PMC8438670 · W3198713176
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study found that miR-139-5p is upregulated in ectopic endometrial stromal cells and promotes their viability, migration, and invasion by directly targeting BBC3.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This study examined whether miR-139-5p contributes to ectopic endometrial stromal cell (ESC) malignant-like behavior in endometriosis, using 15 paired ectopic and non-ectopic endometrial samples plus normal controls to measure miR-139-5p and Bcl-2 binding component 3 (BBC3) expression in ESCs by RT-qPCR and Western blotting. The authors identified BBC3 as a direct miR-139-5p target (TargetScan and dual luciferase reporter assay) and, in ectopic ESCs, showed that inhibiting miR-139-5p decreased viability, migration, and invasion while increasing apoptosis, effects that were reversed by knocking down BBC3. As a limitation, the study used relatively small sample numbers and relied on in vitro functional assays without in vivo confirmation. This paper is centrally about endometriosis — it focuses on how miR-139-5p regulates ectopic ESC viability, migration/invasion, and apoptosis through direct targeting of BBC3.

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Abstract

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

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endometriosis

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