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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Anti-EMT properties of CoQ0 attributed to PI3K/AKT/NFKB/MMP-9 signaling pathway through ROS-mediated apoptosis

Fig. 5

CoQ0 inhibits EMT through downregulation of β-catenin signaling pathways in MDA-MB-231 cells. a CoQ0 inhibited β-catenin nuclear translocation and transcriptional activation. β-catenin levels in total nuclear and cytoplasmic fractions were determined by Western blotting. The cells were incubated with or without CoQ0 (0.5–2 μM) for 24 h. Histone H3 and β-actin were used as internal loading controls for nuclear and cytoplasmic fractions, respectively. b β-catenin mRNA expression was determined by RT-PCR analyses after 6 h treatment with CoQ0 (0.5–2 μM). c Transcriptional activity of β-catenin after treatment with CoQ0 (0.5–2 μM) for 24 h was monitored by luciferase reporter assay. d CoQ0 affects E-cadherin through β-catenin. Cells were incubated with or without CoQ0 (1 μM) for 24 h. Equivalent amounts of proteins were immunoprecipitated with anti-E-cadherin and anti-β-catenin antibodies and visualized by Western blot analysis. e E-cadherin expression was enhanced in cells following treatment with CoQ0 (1 μM) in the presence of the NFκB inhibitor celastrol (0.3 μM) and/or β-catenin inhibitor iCRT5 (5 μM) for 24 h. f β-catenin gene silencing abolished the CoQ0-mediated suppression of EMT. Cells were transfected with a specific β-catenin siRNA or a non-silencing control. Following transfection, the cells were incubated with or without CoQ0 (1 μM) for 24 h. Western blot analyses was performed to measure the expression levels of β-catenin transcriptional target genes such as E-cadherin, Slug, and Snail. The results are presented as the mean ± SD of three independent assays. **p < 0.05, ***p < 0.001 significant compared to control cells

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