Abstract
The development of cancer is a complex phenomenon driven by various extrinsic as well as intrinsic risk factors including epigenetic modifications. These post-translational modifications are encountered in diverse cancer cells and appear for a relatively short span of time. These changes can significantly affect various oncogenic genes and proteins involved in cancer initiation and progression. Histone lysine acetylation and deacetylation processes are controlled by two opposing classes of enzymes that modulate gene regulation either by adding an acetyl moiety on a histone lysine residue by histone lysine acetyltransferases (KATs) or via removing it by histone deacetylases (KDACs). Deregulated KAT activity has been implicated in the development of several diseases including cancer and can be targeted for the development of anti-neoplastic drugs. Here, we describe the predominant epigenetic changes that can affect key KAT superfamily members during carcinogenesis and briefly highlight the pharmacological potential of employing lysine acetyltransferase inhibitors (KATi) for cancer therapy.
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