ArticleJournal of ophthalmology2026
MicroRNA-200c Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells by Activating the Yes-Associated Protein Signaling Pathway.
Article in Journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- MicroRNA-200c Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells by Activating the Yes-Associated Protein Signaling Pathway.Journal of ophthalmology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The aim of the study is to investigate the role and possible mechanism of MicroRNA 200c (MiR-200c) in epithelial-mesenchymal transition (EMT) of Posterior Capsule Opacification (PCO). Methods: Human lens epithelial cells (LECs) were treated with TGFβ2 to induce EMT as a model for PCO. The mRNA levels of miR-200c and EMT markers were examined by real-time quantitative polymerase chain reaction (qPCR). Protein expression levels and mRNA levels of EMT-associated protein/transcriptional coactivators and Yes-associated protein (YAP) were also compared between miR-200c transfected and control cells by western blot analysis and qPCR. The scratch test was applied to detect the migration abilities of cells. Results: The expression level of miR-200c was upregulated in TGFβ2-induced EMT of LECs. Enhanced expression of miR-200c via agomir transfection accelerated both cell migration and the transition to a mesenchymal phenotype. Conversely, miR-200c inhibition using an antagomir effectively suppressed TGFβ2-mediated EMT. Bioinformatics analysis revealed that YAP signaling could be positively regulated by miR-200c, as evidenced by increased levels of YAP observed both in TGFβ2-treated groups and transfected with miR-200c agomir. Inhibition of Yap through the use of YAP-TEAD Inhibitor 1 (Peptide 17) effectively prevented the upregulation of key EMT markers such as FN, vimentin, and transcription factor SNAIL during TGFβ2-induced EMT. Conclusions: MiR-200c promotes EMT and migration in LECs by activating the YAP signaling pathway. MiR-200c may be used as a biomarker for the diagnosis or treatment in PCO.
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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.