miR-223-3p alleviates TGF-β-induced epithelial-mesenchymal transition and extracellular matrix deposition by targeting SP3 in endometrial epithelial cells

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.

Integrative analysis links autophagy to intrauterine adhesion and establishes autophagy-related circRNA-miRNA-mRNA regulatory network

“…The interference efficiency was indicated in Figure 9 . As shown in Figure 10 , the ESCs were treated with TGF-β to mimics the intrauterine adhesion microenvironment to verify the function of hub ARCs through siRNA interference [ 33 ]. The interference efficiency was indicated in Figure 9 .…”

A short peptide encoded by long non‐coding RNA small nucleolar RNA host gene 6 promotes cell migration and epithelial–mesenchymal transition by activating transforming growth factor‐beta/SMAD signaling pathway in human endometrial cells

“…11,12 Moreover, the aberrant migration of endometrial stromal and epithelial cells has been reported to be implicated in the pathogenesis of intrauterine adhesion. 13,14 For instance, Min et al have demonstrated that the proliferative, migratory, invasive, and angiogenic capacities and the percentage of endometrial mesenchymal stem/stromal cells are notably reduced in patients with intrauterine adhesion compared to the healthy control group. 13 Epithelial-mesenchymal transition (EMT) of cells in the endometrium tissues including endometrial epithelial and stromal cells also plays a vital role in multiple essential functions of the uterine endometrium such as decidualization, cyclic regeneration, embryo implantation, cell-cell communication, adhesion, and early pregnancy establishment.…”

“…The migration and invasion of endometrial stromal and epithelial cells are associated with endometrial functions including decidualization, endometrial regeneration, and implantation 11,12 . Moreover, the aberrant migration of endometrial stromal and epithelial cells has been reported to be implicated in the pathogenesis of intrauterine adhesion 13,14 . For instance, Min et al have demonstrated that the proliferative, migratory, invasive, and angiogenic capacities and the percentage of endometrial mesenchymal stem/stromal cells are notably reduced in patients with intrauterine adhesion compared to the healthy control group 13 .…”