ArticleFrontiers in oncology2025
Upregulation of miR-183 inhibits the invasion and migration of endometrial stromal cells in endometriosis patients by downregulating Ezrin.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Engineering the human endometrium at the intersection of development and reproduction.Nature biomedical engineering · 2026Review
- Urinary microRNAs for the non-invasive diagnosis of endometriosis identified by next-generation sequencing and machine learning.Reproductive biology and endocrinology : RB&E · 2026Article
- The Zebrafish miR-183 Family Regulates Endoderm Convergence and Heart Development via S1Pr2 Signaling Pathway.Biomolecules · 2025Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The present study investigated the expression and role of miR-183 in the proliferation, invasion, migration, and apoptosis of endometrial stromal cells in endometriosis patients and the potential involvement of targeting Ezrin. Methods: Normal, non-ectopic, and ectopic endometrial stromal cells (ESCs) were extracted from endometrial samples. RT-qPCR was used to evaluate miR-183 expression levels in endometrial tissue samples. Flow cytometry, cell proliferation assay, adhesion assay and Transwell assays and cell scratch assay were performed to assess cell apoptosis, viability, migration, and invasion of cells transfected with miR-183 inhibitor, miR-183 mimics, or controls. Western blotting was used to determine the expression of the migration-and invasion-related proteins. The expression status of RhoA/ROCK/Ezrin in endometriosis was verified by animal models. Results: miR-183 expression levels were markedly downregulated and RhoA and Ezrin expression levels were upregulated in ectopic endometrial samples. Upregulation of miR-183 expression inhibited cell apoptosis, migration and invasion and promoted cell adhesion in ESCs, but had no significant impact on cell proliferation. miR-183 mimics decreased the expressions of Ezrin, RhoA, RhoC, and Rock. Conclusion: Upregulated expression of miR-183 promoted cell adhesion and suppressed the apoptosis, invasion, and migration of ESCs by downregulating Ezrin. miR-183 may play a suppressor role in endometriosis by downregulating Ezrin to inactivate the Rho/ROCK pathway.
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Registered trials
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