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. 2021 Sep 23;11:700629. doi: 10.3389/fonc.2021.700629

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Copyright © 2021 Patra, Elahi, Armorer, Arunachalam, Omala, Hamid, Ashton, Joyce, Jiao and Pestell

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of metabolic nodes governed by epigenetic modification. Metabolic enzymes and nutrient transporters are governed by modification by DNA methylation and histone modifications. Bidirectional feedback occurs as the metabolic substrates generated in turn regulate epigenetic modifications. α-ketoglutarate is a co-substrate for JHDM (The Jumonji-domain histone demethylase) histone demethylase and the TET family methylcytosine dioxygenases, thereby governing demethylation of histone and other proteins, and DNA. Fumarate, succinate and 2-HG compete with a ketoglutarate. HIF1α (hypoxia inducible factor 1α), KEAP1 (Kelch-like ECH-associated protein 1), NRF2 (nuclear factor erythroid 2-related factor 2), FBP1 (fructose-1,6-bisphosphate isoform 1), TKTL1 (transketolase (TKT) like-1 gene), SAM (S-adenosyl methionine), TCA (tricarboxylic acid), The abundance of GLUT3 and GLUT1 are regulated by CAV-1 and Derlin3 respectively.