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. 2019 Apr 11;11:2997–3007. doi: 10.2147/CMAR.S199368

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© 2019 Zhu et al.

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BCL11A promotes the breast cancer cell stemness and epithelial-mesenchymal transition by activating the Wnt/b-catenin pathway. (A) Relative C-myc, fibronectin, β-catenin, CD44, cyclinD1, slug, and snail expression level between BCL11A-modulating cells and controls of MDA-MB-231 and MCF7 was characterized by Western blotting. (B) The C-myc, CD44, fibronectin, β-catenin, cyclinD1, slug, and snail expression level was effectively decreased by Dkk1, a Wnt inhibitor, in BCL11A-overexpressing MCF-7 cells, whereas effectively increased by Wnt3a, a Wnt agonist, in MDA-MB-231 cells transfected with shBCL11A. (C) Wnt3a significantly promoted the formation of more spheres, whereas the Wnt inhibitor DKK1 reversed this trend and reduced tumor spheres number. All the data was shown as the mean ± SD, and three independent experiments were performed (**p<0.01; *p<0.05). (D) BCL11A and CD44 expression were further confirmed in xenograft tumors of nude mice through immunohistochemistry, and representative images were shown. Original magnification, 200×.