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. 2017 Nov 7;17(1):783–788. doi: 10.3892/mmr.2017.8007

Figure 3.

Figure 3.

ZO-1 is a direct target of miR-103 in colorectal cancer. (A) The miR-103 wild-type binding sequence or its mutated form was inserted into the C-terminal of the luciferase gene to generate the pGL3-ZO-1-3′ UTR or pGL3-ZO-1-mut-3′ UTR plasmids, respectively. (B) miR-103 targeted the wild type but not the mutant 3′ UTR of ZO-1. The data represent the mean ± standard deviation. *P<0.05 vs. NC. (C) Western blotting and densitometric analysis revealed that miR-103 overexpression inhibited the protein expression levels of ZO-1 in SW620 cells. SW620 cells were transfected with the miR-103 mimic, mimic control or NC. β-actin served as the loading control. The data represent the mean ± standard deviation. *P<0.05 vs. NC; #P<0.05 vs. CON. (D) Western blotting and densitometric analysis demonstrated that knockdown of miR-103 upregulated the protein expression levels of ZO-1 in SW620 cells. SW620 cells were transfected with the miR-103 inhibitor, inhibitor control or NC. The data represent the mean ± standard deviation. *P<0.05 vs. NC; #P<0.05 vs. CON. ZO-1, zonula occuldens-1; miR-103, microRNA-103; 3′UTR, 3′-untranslated region; NC, transfection negative control; CON, untransfected control.