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. 2018 Jul 18;16(3):2235–2242. doi: 10.3892/etm.2018.6461

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Copyright: © Bai 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 4. — EZR-AS1 protects β-catenin from degradation and activates the Wnt/β-catenin pathway in BC cells. (A) RNA immunoprecipitation assays indicated that EZR-AS1 was enriched by anti-β-catenin in MCF7 and MDA-MB-231 cells. (B) An RNA pull-down assay indicated that β-catenin was precipitated by biotin-labeled EZR-AS1. (C) EZR-AS1 overexpression prevented β-catenin degradation in MCF7 cells. (D) Western blotting was performed to assess the effect of EZR-AS1 knockdown on nuclear β-catenin, MYC, SOX4 and Cyclin D1 expression in MCF7 and MDA-MB-231 cells. (E) Correlation between EZR-AS1 and MYC or SOX4 in BC tissues. *P<0.05 vs. IgG. All data are presented as the mean ± standard deviation of three independent experiments. BC, breast cancer; SOX, SRY box; oe, overexpression; si, small interfering RNA; NC, negative control; Ig, immunoglobulin.