Journal of ophthalmology · 2026
MicroRNA-200c Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells by Activating the Yes-Associated Protein Signaling Pathway.
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Wei Yin-Juan, Liu Yi-An-Zhu, Dai Ying, Nan Li, Song Hui, Li Jun
Аннотация
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.
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.