{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T08:04:30Z","timestamp":1784016270738,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"vor","delay-in-days":194,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004945","name":"Nankai University","doi-asserted-by":"publisher","award":["NKYKK202211"],"award-info":[{"award-number":["NKYKK202211"]}],"id":[{"id":"10.13039\/501100004945","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["62272248"],"award-info":[{"award-number":["62272248"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Ophthalmology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>The aim of the study is to investigate the role and possible mechanism of MicroRNA 200c (MiR\u2010200c) in epithelial\u2013mesenchymal transition (EMT) of Posterior Capsule Opacification (PCO).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Human lens epithelial cells (LECs) were treated with TGF\u03b22 to induce EMT as a model for PCO. The mRNA levels of miR\u2010200c and EMT markers were examined by real\u2010time quantitative polymerase chain reaction (qPCR). Protein expression levels and mRNA levels of EMT\u2010associated protein\/transcriptional coactivators and Yes\u2010associated protein (YAP) were also compared between miR\u2010200c transfected and control cells by western blot analysis and qPCR. The scratch test was applied to detect the migration abilities of cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The expression level of miR\u2010200c was upregulated in TGF\u03b22\u2010induced EMT of LECs. Enhanced expression of miR\u2010200c via agomir transfection accelerated both cell migration and the transition to a mesenchymal phenotype. Conversely, miR\u2010200c inhibition using an antagomir effectively suppressed TGF\u03b22\u2010mediated EMT. Bioinformatics analysis revealed that YAP signaling could be positively regulated by miR\u2010200c, as evidenced by increased levels of YAP observed both in TGF\u03b22\u2010treated groups and transfected with miR\u2010200c agomir. Inhibition of Yap through the use of YAP\u2010TEAD Inhibitor 1 (Peptide 17) effectively prevented the upregulation of key EMT markers such as FN, vimentin, and transcription factor SNAIL during TGF\u03b22\u2010induced EMT.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>MiR\u2010200c promotes EMT and migration in LECs by activating the YAP signaling pathway. MiR\u2010200c may be used as a biomarker for the diagnosis or treatment in PCO.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/joph\/5384666","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T07:20:42Z","timestamp":1784013642000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["MicroRNA\u2010200c Promotes Epithelial\u2013Mesenchymal Transition of Lens Epithelial Cells by Activating the Yes\u2010Associated Protein Signaling 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