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BACKGROUND In view of the high incidence of posterior capsule opacification (PCO) and the effects of TGF-β signaling on the epithelial-mesenchymal transition (EMT) of human lens epithelial cells (LECs), our study aimed to explore the mechanism of the function of TGF-β signaling in LECs EMT. MATERIAL AND METHODS Human lens epithelial cells (HLEC-h3) were treated with TGF-β, ILK siRNA, ILK inhibitor, and NF-κB inhibitor to study the effects of TGF-β, ILK, and NF-κB on cell migration and EMT. Cell migration assay was used to measure cell migration ability. Western blot was performed to detect the expression of ILK, E-cadherin, and a-SMA at the protein level. QRT-PCR was used to detect the expression of ILK at the mRNA level. RESULTS Compared with control cells, TGF-β treatment increased the expression level of ILK HLEC-h3, promoted migration of HLEC-h3 cells, increased the expression level of E-cadherin protein, and decreased the expression level of a-SMA protein. However, treatment with ILK siRNA, ILK inhibitor, and NF-κB inhibitor reversed the effects of TGF-β on HLEC-h3 cells. CONCLUSIONS TGF-β-stimulated ILK regulates the migration and EMT of human LECs via NF-κB.

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Transforming Growth Factor β1 (TGF-β1)-Stimulated Integrin-Linked Kinase (ILK) Regulates Migration and Epithelial-Mesenchymal Transition (EMT) of Human Lens Epithelial Cells via Nuclear Factor κB (NF-κB)