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. 2017 Aug 29;7:9842. doi: 10.1038/s41598-017-10555-z

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Constitutively Active AKT Abolishes the Synergistic Effect of Treatment with Tamoxifen and PI3K inhibitor. (A) AKT expression level was measured by Western blot analysis in MCF-7 cells without transfection (parental), cells transfected with empty vector (MCF-7/mock), and cells transfected with myristoylated AKT (MCF-7/AKT). (B) Comparison of p-GSK3b, pp-70S6K, and p-4EBP1 expression levels between MCF-7/mock and MCF-7/AKT cells treated with control (CTL), tamoxifen (T, 8 µM), alpelisib (BYL, 5 µM), or tamoxifen and alpelisib (T + BYL, 8 µM + 5 µM) at 3, 8, and 24 hours. Fa plots of combination indices for treatment with T + BYL in MCF-7/mock (C) or MCF-7/AKT (D) cells and treatment with T + BKM in MCF-7/mock (E) or MCF-7/AKT (F) cells.