Authors
Yin-Juan Wei, Yi-An-Zhu Liu, Ying Dai, Li Nan, Hui Song, Jun Li
Published in
Journal of ophthalmology. Volume 2026. Pages 5384666. Epub Jul 14, 2026.
Abstract
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).
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.
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.
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.
PMID:
42454080
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.
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