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. 2020 Oct 6;11(10):831. doi: 10.1038/s41419-020-03037-0

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© The Author(s) 2020

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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Fig. 8 — a Functional associations of the regulatory networks of CD44-correlated genes from analysis of STRING data are presented. b Scheme summarizing the proposed mechanism by which CD44 drives resistance to PI3Kα in luminal breast cancer. Upregulation of CD44 and the interaction of CD44 with HA leads to interconnected feedback loops consisting of CD44-ESRP1-Has2-ER, generating robust compensatory activation of the Src-ERK-Ezrin signaling cascade and dynamic regulation of the transition from a sensitive to resistant phenotype. The combination of PI3Kα inhibition with CD44 or HA suppression prevents this effect by blocking the Src/MAPK axis, resulting in superior antitumor activity.