[Retracted] IGF-1 Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells That Is Conferred by miR-3666 Loss

Figure 6

IGF-1 was necessary for promoting the EMT effects of the miR-3666 inhibitor. (a) qRT-PCR was used to detect the silencing efficiency of the miR-3666 inhibitor. n = 6. (b–d) Silencing IGF-1 reversed miR-3666 inhibitor-induced mRNA expression of IGF-1, CDH1, and vimentin, which was measured by qRT-PCR. n = 6. (e) Using western blot to investigate the effect of sh-IGF-1 with or without the miR-3666 inhibitor on the level of IGF-1, E-cadherin, and vimentin protein. (f) Analysis of western blot, n = 4. (g) Wound-healing tests showed that inhibition of IGF-1 ablated the cell migration induced by the miR-3666 inhibitor. (h) Analysis of wound-healing assay, n = 6. (i) Transwell assay showed that the miR-3666 inhibitor-induced invasion ability of HLECs was inhibited by sh-IGF-1. (j) Analysis of Transwell assay, n = 6. (k) EdU staining showed that silencing of IGF-1 inhibited cell proliferation induced by the miR-3666 inhibitor. (l) Analysis of EdU staining, n = 6. ; .

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