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. 2016 Aug 11;10:73. doi: 10.1186/s12918-016-0316-x

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© The Author(s). 2016

Open AccessThis 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 — Signaling network of drug-induced glioma differentiation. Signaling pathways involved in the regulation of glioma differentiation during glioma differentiation. Elevation of cAMP level by cholera toxin (CT), can induce glioma cell differentiation, which is mediated by CREB phosphorylation at Ser-133 in a PKA dependent manner [2]. cAMP/PKA signaling can also inhibit the PI3K/AKT pathway, leading to activation of the downstream molecule GSK-3β and subsequent degradation of cyclin D1 [3]. Additionally, the IL-6/JAK2/STAT3 pathway, which is activated by increased cAMP levels, is also involved in glioma cell differentiation [4]. Glial fibrillary acidic protein (GFAP) is used as a reliable marker for evaluating the differentiation of glioma cells