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. 2019 Mar 19;10(4):268. doi: 10.1038/s41419-019-1505-5

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© The Author(s) 2019

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. 1 — Schematic representation of activated signaling cascades in GSCs following treatment with SM; NF-kB activation promotes an autocrine/paracrine TNFα/IL6 signaling which in turn activates AKT/EZH2 and STAT3, consequently promoting self-renewal and therapeutic resistance. On the other hand, the combination of SM with EZH2 inhibitors results in cell death and GSCs depletion