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. 2021 Jan 13;14:7. doi: 10.1186/s13072-020-00380-6

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 6 — Proposed differential signaling schema comparing PNFs and CNFs. Although both RAS/MEK/ERK and RAS/MKK3/P38 signaling occurs in both tumor types, RAS activation results in differential signaling strength and fidelity through RAS/MEK in PNFs (left panel) and, alternatively, RAS/MKK3/P38 in CNFs (right panel). CNFs divert RAS activation through MKK3 thereby enhancing the cellular response to stress and inflammation that is mediated by MKK3/p38, whereas the downstream impact in RAS/MEK dependent PNFs is unchecked growth and proliferation (left). CNFs still maintain growth and proliferation signaling through RAS/ERK or p38/ERK, but strongly exhibit a pro-inflammatory phenotype and are characterized by broad chromatin remodeling (right)