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Fig. 2 | Clinical Epigenetics

Fig. 2

From: Crosstalk between DNA methylation and hypoxia in acute myeloid leukaemia

Fig. 2

Complex interactions between hypoxia and DNA methylation. Hypoxia may influence DNA methylation via direct effects on TET activity, altered transcription, or metabolic reprogramming. DNA methylation may also influence hypoxia responses. A Oxygen is an essential co-factor for TET enzymes, and hypoxia reduces TET-mediated DNA hydroxymethylation in some cancers. B In certain cell types, hypoxia-inducible factors (HIFα, HIFβ) bind to hypoxia-responsive elements (HREs) in TET and DNMT promoters to induce their expression. C In hypoxia, cancer cells can induce a metabolic switch from oxidative phosphorylation to glutamine metabolism. In IDH wild-type cells, upregulated glutamine metabolism has been associated with production of 2-HG which can inhibit TET enzymes. D DNA methylation can prevent the binding of HIF complexes to HREs, altering transcriptional responses induced by hypoxia

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