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. 2019 Jul 4;20:375. doi: 10.1186/s12859-019-2970-7

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© Sai and Kong. 2019

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Glioma differentiation signaling network. Cholera toxin (purple) acts as a principal input to the system, inducing glioma cell differentiation via multiple pathways, the PKA/CREB [13], P13K/AKT/pGSK3 β/cyclin D1 [14], and IL6/JAK2/STAT3 [15] pathways. GFAP (pink) serves as the differentiation marker, measuring the extent to which glioma cells differentiate into normal glia-like cells