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. 2021 May 20;13(5):762. doi: 10.3390/pharmaceutics13050762

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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TCA cycle, main oncometabolites and effects on cancer biology. An altered tricarboxylic acid (TCA) cycle due to gain-of-function mutations (*) in isocitrate dehydrogenase (IDH) and loss-of-function mutations (X) in succinate dehydrogenase (SDH) and fumarate hydratase (FH), produces high levels of 2-hydroxyglutarate (2-HG), succinate and fumarate, respectively, that act as oncometabolites by pleiotropic mechanisms. PHDs: prolyl-hydroxylases; SUCNR1: succinate receptor 1; mtROS: mitochondrial reactive oxygen species; KDMs: histone lysine demethylases; TET: ten-eleven translocation proteins; HIF-1α: hypoxia-induced transcriptional factor; NHEJ: non-homologous end-joining; Cdc42: cell division control protein 42; MLK3: mixed lineage kinase 3; BCL2: B-cell lymphoma 2; EMT: epithelial mesenchymal transition.