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. 2017 Mar 30;7:46. doi: 10.3389/fonc.2017.00046

Figure 3.

Figure 3

Redox-dependent epigenetic regulation and oncogenesis. Left panel: transient Nrf2 activation is an important component of the adaptive metabolic responses to oxidative stressors, accompanied by epigenetic changes, which promote homeostatic restoration of redox equilibrium. Middle panel: multiple oxidative challenges increase the potential for DNA mutations, including mutations of growth factor signaling pathway components, which can lead to sustained Nrf2 activation, resulting in abnormal redox and epigenetic status. Right panel: methionine-independent and methionine-dependent states can alternatively emerge from oncogenesis, depending upon the level of MS activity, which is influenced by the ratio of cystine/cysteine uptake vs. transsulfuration. Abbreviations: GSH, glutathione; GSSG, glutathione disulfide; MS, methionine synthase; Nrf2, nuclear factor (erythroid-derived 2)-like 2.