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. 2019 Feb 18;38:85. doi: 10.1186/s13046-019-1075-5

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© The Author(s). 2019

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. 6 — Schematic model of PDGFRβ switch upon MEK1/2 or JAK2 inhibition in TNBC cells. Under normal physiological condition, PDGFRβ expression is transcriptionally controlled by MYC through MAPK signaling and its protein level is controlled through JAK2 mediated proteolysis (left panel). Upon targeted inhibition of these signaling pathways (i.e. AZD6244, MEK162, BSK805 or AZD1480) results in accumulation of PDGFRβ, driving resistance in breast cancer (right panel), GF: Growth factor; GFR: Growth factor receptor