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. 2016 Sep 26;35:151. doi: 10.1186/s13046-016-0422-z

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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. 5 — The intracellular pathways in EGF-induced AREG expression. The EGF-induced AREG mRNA (a) and protein (b) expression was reduced after EGFR-kinase inhibition in all cell lines, while it showed no reduction after ErbB2-kinase inhibition and was differently affected by the MAPK inhibitors. a Whereas MEK-inhibition reduced EGF-induced AREG mRNA expression in all the three cell lines, p38- and JNK-inhibition did not. PI3K-inhibition increased EGF-induced AREG expression in all cell lines. b EGF-induced AREG protein secretion could be totally blocked by EGFR- inhibition. Whereas MEK- and JNK-inhibition profoundly decrease EGF-induced AREG expression in all cell lines, p38-inhibition had no effect. The PI3K-inhibitor reduced EGF-induced AREG production in the conventional OSCC cell line D2 and E10, but had no effect on the basaloid OSSC cell line C12. The ErbB-2- inhibition inhibited the AREG increase in E10 cell line, only. *represents significant difference with EGF stimulation groups without inhibitors (student’s t-test)