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. 2023 Mar 13;199(1):13–23. doi: 10.1007/s10549-023-06895-2

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© The Author(s) 2023

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — p110α protein levels in breast cancer cell lines treated with MEN1611 and other PI3K inhibitors. Analysis of p110α protein and pAKT levels in breast cancer cell lines treated with MEN1611, taselisib and alpelisib. Cell lines were treated for 24 h with the indicated concentrations and analyzed by capillary immunoblot. The levels of p110α were normalized to GAPDH and expressed as percentage of the control. The inhibition of the PI3K signaling was evaluated by determination of pAKT levels. Results are presented as mean ± SD (N = 3) and for each experiment a representative lane view image was showed. Effect of MEN1611, BYL719 and taselisib on p110α protein level and downstream signalling in PIK3CA mutated, and (a) wild-type breast cancer cell lines (b). Effect of MEN1611 on p110α protein level in HCC1806 (PIK3CA wt) cell line treated with a wide range of concentration (c). Effect of MEN1611 on p110α protein level in the non-tumorigenic human breast epithelial cell line MCF10A (d)