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. 2018 Jun 11;16(2):2462–2470. doi: 10.3892/ol.2018.8940

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Role of miR-23a transfection in regulating the EMT in intraocular tumor cells. RT-qPCR detection of the role of miR-23a transfection in (A) human choroidal melanoma cell strains OCM-1, (D) human retinoblastoma cell strains WERI-RB1 and (G) Y79 in regulating the expression of E-cadherin at the level of mRNA. The inhibitor transfection of miR-23a significantly decreased the mRNA of E-cadherin relative to the control group (*p<0.05) while vimentin increased significantly (*p<0.05). The mimic transfection significantly increased E-cadherin (*p<0.05) and significantly decreased vimentin (*p<0.05). Western blot analysis was used to detect the effect of miR-23a transfection of (B) human choroidal melanoma cell strains OCM-1, (E) human retinoblastoma cell strains WERI-RB1 and (H) Y79 on the expression of the proteins related to EMT. The miR-23a mimic transfection increased the expression of the epithelial cell marker, E-cadherin protein whereas the expression levels of the mesenchymal cell-labeled proteins of N-cadherin and vimentin decreased significantly. The miR-23a inhibitor transfection group exhibited an opposite acting trend. The proteins related to EMT were subjected to an immunofluorescence analysis after (C) the human choroidal melanoma cell strains OCM-1, (F) the human retinoblastoma cell strains WERI-RB1 and (I) Y79 were transfected with miR-23a. The expression of the epithelial marker E-cadherin in the inhibitor transfection group decreased while the expression of the mesenchyme-labeled vimentin increased. Vimentin decreased and E-cadherin increased in the mimic transfection group. EMT, epithelial-mesenchymal transition.