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. 2018 Jan 4;10:2. doi: 10.1186/s13073-017-0511-4

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© The Author(s). 2018

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. 3 — Modulation of the Ras pathway phenotypes of MEK/ERK phosphorylation and anchorage-independent growth by FOXO3, NCOA3, and TCF7L2. Soft agar assays (a) and growth curves in normal medium (b) in stable shRNA lines of NCOA3, FOXO3, and TCF7L2 in DLD-1 cells (KRAS G13D). The impact of NCOA3, FOXO3, and TCF7L2 perturbation on pMEK and pERK in relation to MEK and ERK, respectively, were quantified by NanoPro analysis in DLD-1 (KRAS G13D) (c, e) and RKO (BRAF V600E) (d, f) cells with shKRAS and shBRAF as positive controls. Each experiment was performed at least twice with three technical replicates with statistical analysis by Student’s t-test where ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05