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. 2019 Jan 16;38(18):3504–3520. doi: 10.1038/s41388-018-0632-2

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© The Author(s) 2019

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

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Fig. 1 — Differential cell growth response upon rival oncogene expression. The rival oncogene was induced with doxycycline (50–100 ng/ml) and subjected for 6 days cell viability assays using cell-titer-glow reagent. a A panel of four isogeneic stable NRAS(Q61)/Tet-On BRAF(V600E) and five BRAF(V600E)/Tet-On-NRAS(Q61R) mutant cell lines and an immortalized primary human melanocyte line (Pmel) were assayed for cell viability at fifth day following rival oncogene induction with doxycycline. Cell lines showing antagonism such as b two NRAS(Q61R)/Tet-On-BRAF(V600E) and c two BRAF(V600E)/Tet-On-NRAS(Q61R). Cell lines showing cooperativity/neutral such as d one BRAF(V600E)/Tet-On-NRAS(Q61R) and one NRAS(Q61R)/Tet-On-BRAF(V600E). The protein expression was confirmed by western blotting. For each cell line, cell viability was performed independently more than three times in triplicates. Student’s t test, doxycycline vs. no-doxycycline, ^◇p ≤ 0.05