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. 2022 Jan 12;11(1):2. doi: 10.1038/s41389-022-00378-7

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© The Author(s) 2022

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. 6 — In MGMT-deficient GBMs, after growth factors bind to their cell surface receptors, Cx43 is expected to recruit p110β/p85 signaling complexes to the membrane through a selective binding to p110β. This in turn activates PI3K/AKT signaling and induces MGMT-independent TMZ resistance. It is also expected that αCT1, a mimetic peptide of Cx43 CT, blocks the interaction between Cx43 and p110β, thereby inactivating p110β and overcoming TMZ resistance. Moreover, p110β-selective inhibitors TGX-221 and GSK2636771, which block p110β kinase activity, synergize with αCT1 to restore TMZ sensitivity in MGMT-deficient GBMs.