ArticleOpen medicine (Warsaw, Poland)2022
miR-223-3p alleviates TGF-β-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Single cell multiomics revealed fibrotic trajectories of endometrial cells and interaction with the pro-fibrotic macrophages in intrauterine adhesion.Genome medicine · 2026Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.Frontiers in immunology · 2026Article
- Single-cell RNA sequencing of endometrium uncovers dynamic characteristics and dysregulation of perivascular CD9Stem cell research & therapy · 2025Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomics of tissue exosomes to investigate miR-195-5p's amelioration of endometrial fibrosis via the YAP-Smad7 pathway: an animal study.Journal of translational medicine · 2024Article
- Altered Expression of CirculatingInternational journal of fertility & sterility · 2024Article
- TGF-β1 overexpression in severe COVID-19 survivors and its implications for early-phase fibrotic abnormalities and long-term functional impairment.Frontiers in immunology · 2024Article
- Article
Corrections and comments
- Retraction · 2023-12-31Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Third Party Involvement · Duplication of/in Image · · See also: https://pubpeer.com/publications/2F25413A3CAB734078F3E5AA34BD77
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrauterine adhesion (IUA) is the clinical manifestation of endometrial fibrosis. The dysregulation of microRNAs (miRNAs) has been confirmed to implicate in a diversity of human diseases, including IUA. Nevertheless, the specific function of miR-223-3p in IUA remains to be clarified. Reverse transcription quantitative polymerase chain reaction analysis displayed the downregulation of miR-223-3p in IUA tissues and endometrial epithelial cells (EECs). Results from wound healing assay, Transwell assay and western blotting showed that TGF-β facilitated the migration and invasion of EECs and induced epithelial-mesenchymal transition (EMT) process as well as extracellular matrix (ECM) deposition. Overexpression of miR-223-3p in EECs was shown to suppress the effects induced by TGF-β. Bioinformatics analysis and luciferase reporter assay revealed the binding relation between miR-223-3p and SP3. SP3 was highly expressed in IUA and its expression was inversely correlated with miR-223-3p expression in IUA tissue samples. Additionally, upregulation of SP3 reversed the influence of miR-223-3p on the phenotypes of EECs. In conclusion, miR-223-3p alleviates TGF-β-induced cell migration, invasion, EMT process and ECM deposition in EECs by targeting SP3.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.