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. 2017 Oct 4;17:86. doi: 10.1186/s12935-017-0457-z

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© The Author(s) 2017

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. 4 — Dual EGFR and BRAF blockade prevents EGFR feedback activation and induces prolonged suppression of ERK signaling in BRAF V600E thyroid carcinoma cells. a AKT, phosphoAKT, EGFR, phosphoEGFR, ERK and phosphoERK immunoblot analysis in BRAF V600E FRO, BCPAP, and BHT101 thyroid carcinoma cell lines exposed to 10 μM PLX4032 or 10 μM gefitinib or the combination of both agents for 4 (BCPAP cells), 6 (FRO cells) or 8 (BHT101 cells) h. b ERK and phosphoERK immunoblot analysis in BRAF V600E FRO, BCPAP and BHT101 thyroid carcinoma cell lines exposed to 10 μM PLX4032 or 10 μM gefitinib or the combination of both agents for 15 h (24 h in BHT101 cells)