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. 2018 Feb 23;8:41. doi: 10.3389/fonc.2018.00041

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Copyright © 2018 Sun, Chen and Deshpande.

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 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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Epigenetic modifiers in cancer as clinical targets: (A) tumor suppressor genes (TSG) may be silenced by chromatin compaction resulting from DNA methylation or histone deacetylation, or repressive histone methylation. DNA methyltransferase (DNMT) inhibitors, demethylating agents, histone deacetylase (HDAC) inhibitors, or inhibitors of repressive histone modifying complexes such as PRC2 may restore the expression of these TSGs. (B) In contrast, oncogene activation by means of activation-associated histone hypermethylation, or histone hyperacetylation could be countered with the use of selective histone methyltransferase (HMT) or acetyltransferase histone acetyltransferase (HAT) inhibitors. Additionally, readers that recruit these activation-associated marks, such as the AF10 PZP domain, the AF9 or ENL YEATS domain, and the BRD4 bromodomains, and recruit transcriptional complexes present targets for pharmacological intervention.