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. 2019 Dec 10;122(1):72–81. doi: 10.1038/s41416-019-0628-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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Fig. 4 — Vemurafenib-resistant cell clones exhibit decreased glycolytic metabolism and enhanced mitochondrial anaplerotic metabolism. a Resistant R6 cells produce significantly less lactate^E and show a significantly lower glucose uptake in comparison to A375 cells. b R6 cells produce significantly less glutamate ([4]-[4,5] glutamate) than sensitive cells but maintain similar fumarate and acetate levels despite a lower glucose consumption rate, indicating a potential upregulation in TCA activity non-glutamine or PDH dependent. Anaplerotic TCA activity is significantly higher in R6 cells compared to the parental clone (p = 0.01). c The molecular analysis of three biological replicates from A375 and R6 cells revealed a lower GLUT-1 and GLS (KGA and GAC isoforms) expression and a higher PC expression in vemurafenib-resistant cells in comparison to sensitive cells. **p < 0.01.