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. 2012 Nov 8;104(1):48–54. doi: 10.1111/cas.12030

Figure 2.

Figure 2

ZEB1 was directly suppressed by miR‐150 in ESCC. (A) MiR‐150 binding sites in the ZEB1 3′‐UTR. Putative conserved target sites in 3′‐UTR were identified using in silico miR target prediction tools. (B) Luciferase assays of premiR‐150 transfected TE‐8 cells. The error bars represent the SD from eight replicates. Left bar: ZEB1 3′UTR luciferase vector only. Middle bar: ZEB1 3′‐UTR luciferase vector + premiR‐nc. Right bar: ZEB1 3′‐UTR luciferase vector + premiR‐150. (C) Western blotting of ZEB1, E‐cadherin, and vimentin protein in premiR‐150 transfected TE‐8 cells. These proteins were normalized to the level of beta‐actin. Bar graph shows miR‐150 expression in in the premiR‐150‐treated group and control cell groups (*P < 0.05). (D) MiR‐150 and ZEB1 expression levels in ESCC samples were measured by real‐time RT‐PCR. ZEB1 expression was inversely correlated with the expression of miR‐150 (correlation coefficient, ‐0.40). MiR‐150 and ZEB1 data were normalized to RNU6B and GAPDH.