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. 2021 Jun 10;22(12):6264. doi: 10.3390/ijms22126264

Figure 2.

Figure 2

Impact of NO in DNA methylation (A), histone methylation (B), histone acetylation (C) and histone phosphorylation (D). DNA methyltransferases (DNMT) enzymes are responsible for methylating DNA cytosine residues. Genes with low promoter cytosine methylation are expressed (A1), but upregulation of DNMT protein expression and activity by NO leads to increased DNA methylation at promoter regions and repression of downstream associated targets (A2). NO inhibits histone deacetylases (HDAC) by S-nitrosation increasing acetylation level causing harmful ectopic gene expression, oncogenic processes, pathophysiological conditions induction and enzymatic function weakness (B). NO inhibits H3K9me2 lysine demethylase 3A (KDM3A) leading to decreased histone methylation status and tumor growth (C1). Nonetheless, NO promotes Oct4 expression and CSCs maintenance through inhibiting H3K36me2 demethylase KDM2A (C2). NO induces genomic DNA double-strand breaks and tumor progression (D). Acetylation, Ac; lysine demethylase 2A, KDM2A; methylation, Me; phosphorylation, P.