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Fig. 3 | Journal of Ovarian Research

Fig. 3

From: MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

Fig. 3

MiR-1307 down-regulated the direct target ING5 expression in vitro. a Bioinformatics results. The 3’-untranslated region (3’-UTR) of ING5 contains a potential miRNA-binding site for miR-1307. We inserted the ING5 UTR (1–1037 bp) with either a wild-type or mutant miR-1307 target sequence downstream of the firefly lucierase gene into the pGL3-control vector (Promega) to create the pGL3-ING5 UTR WT or the pGL3-ING5 UTR Mut construct, respectively. b Luciferase reporter assay results. The pGL3-ING5 UTR WT, pGL3-ING5 UTR Mut and pGL3 constructs were individually transfected into A2780 cells. MiR-1307 significantly decreased the relative luciferase activity of the wild-type ING5 3’UTR compared with the mutant ING5 3’UTR. c The ING5 protein expression level following different miR-1307 treatment in A2780/Taxol and A2780 cells by using western blot. The results showed the ING5 protein expression level was lower in A2780/Taxol cells than that in A2780 cells (P < 0.05). d The ING5 protein expression level following different miR-1307 treatment in ovarian cancer cells by using western blot. The ING5 protein expression level was lower treated with miR-1307 mimics than that treated with miRNA con in the A2780 or SKOV3 cells (P < 0.05, respectively). Moreover, the ING5 protein expression level was higher treated with miR-1307 ASO than that treated with ASO con in the A2780 or SKOV3 cells (P < 0.05, respectively). Results are representative of at least three separate experiments. Data are expressed as the mean ± standard deviation. Data from three experimental determinations and bars indicate the SD (*P < 0.05, **P < 0.01)

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