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. 2018 Apr 19;5(3):e1432260. doi: 10.1080/23723556.2018.1432260

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This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 1. — Upregulation of ADHFE1 promotes accumulation of D-2-hydroxyglutarate in breast tumors. c-Myc signaling increases D-2-hydroxyglutarate (D-2HG) by increasing the availability of both the substrates [4-hydroxybutyrate (4-HB) and α-ketoglutarate (α-KG)] and iron for the ADHFE1 enzyme. ADHFE1 and D-2HG up-regulate reductive carboxylation of glutamine-derived α-KG, reactive oxygen species (ROS) formation, and histone methylation at H3K4me3, leading to increased acetyl coenzyme A (acetyl CoA) and fatty acid synthesis and epithelial-mesenchymal transition (EMT). SSA, succinic semialdehyde; H3K4me3, histone trimethylation at histone H3, lysine 4.