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. 2020 May 1;22:39. doi: 10.1186/s13058-020-01277-8

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© The Author(s) 2020

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. 8 — GR Ser134 phosphorylation creates a feedforward signaling loop that potentiates further activation of the p38 MAPK pathway downstream of TGFβ1 in TNBC models. Schematic of the conserved three kinase cascade that represents the p38 MAPK module (i.e., MAP3K5, MEK3/6, and p38 MAPK) and known cooperation between 14-3-3ζ and MAP3K5 [50]. Cellular stress as well as TME-derived factors (TGFβ1) input to activation of SMADs and p38 MAPK signaling, resulting in phosphorylation of GR on Ser134. Ligand-independent pS134-GR target genes include key components of the p38 MAPK pathway (MAP3K5) needed for intact p38 signaling. Potential cooperation of 14-3-3ζ and pS134-GR with the SMAD-dependent arm of the TGFβ1 signaling pathway is shown (dotted two-way arch under question mark).