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. 2019 Jul 17;9:10369. doi: 10.1038/s41598-019-46594-x

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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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DNFA supports survival in drug-resistant melanoma cells. (a,b) HT-144BR is a BRAF inhibitor resistant HT-144 cell line, which was derived after prolonged treatment with vemurafenib (2 μM) in 10% FBS medium for three months. Viability of HT-144 and HT-144BR cells responding to vemurafenib or ASO4 treatment in 10% FBS medium was assessed by cell titer-glo assay. (c,d) LOXIMVIBR is the BRAF inhibitor resistant LOXIMVI cell line, which was derived after prolonged treatment with vemurafenib (2 μM) in 10% FBS medium for three months. Viability of LOXIMVI and LOXIMVIBR cells responding to vemurafenib or ASO-4 treatment was assessed by cell titer-glo assay in 10% FBS medium. (e–h) HT-144 and HT-144BR cells were co-treated with FASN inhibitor (FASNi) GSK 2194069 and SCD inhibitor (SCDi) MF-438 in 10% FBS medium or 10% FBS medium with vemurafenib (2 μM). (e,g) Cell viability was measured by cell titer-glo assay six days after treatment. (f,h) The combination responses for two DNFA enzyme inhibitors were evaluated with the Bliss independence model. Positive Bliss scores indicate synergy between two drugs.