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. 2020 Oct 27;39:224. doi: 10.1186/s13046-020-01733-5

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Impacts of intracellular metabolites on HIF-α stability through epigenetic regulation. In hypoxic tumors, rapid proliferation requires lots of intracellular metabolites to build macromolecules, including nucleotides and proteins. Up-regulated glycolysis sustains the demands of tumor cells for intracellular metabolites. HIF target genes encoding special enzymes are activated to produce various enzymatic proteins, such as PDK1/2, enolase 1 (ENO1), hexokinase 2 (HK2) and so on, which leading to elevated intracellular metabolites, in turn, these metabolites including succinate, fumarate, pyruvate, lactate and oxaloacetate etc. and associated pathways involved enzymes such as PI3K, PKB, promote HIF proteins stability with PHD loss-of-function. More, p53, β-catenin and so on, could also affect HIFs stability. PFKM: phosphofructokinase, muscle; GLUT1: glucose transporter 1; PKM2: pyruvate kinase isozymes M2; LDHA: lactate dehydrogenase A; ERK: extracellular signal-regulated kinases; PGM1: phosphoglucomutase-1; G6PDH: glucose-6-phosphate dehydrogenase; Aldo: Aldosterone; MCT4: monocarboxylate transporter 4; F6P: fructose 6-phosphate; FBP: fructose-1,6-bisphosphate; G3P: glycerol-3-phosphate; 3PG: 3-phosphoglyceric acid; 2PG: 3-phosphoglyceric acid; PEP: phospho enol pyruvate