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Epigenetic modifications of DNA-template processes have been a rising field of study for cancer therapy in the past 15 years. Epigenetic modifications refer to the reversible changes in the genome of cells that do not involve any alteration in the DNA sequence. As promising preclinical and clinical results support the potential role of drugs targeting epigenetics in cancer therapy, the field of cancer epigenetics is gaining heightened attention. Increasing evidence suggests the epigenetics is as important as that of genetic mutations, deletions, rearrangements, and gene amplifications in cancer initiation, progression, treatment and prognosis. To date, there are three major epigenetic machineries that are known to be related to cancers: altered histone acetylations, modified DNA methylations, and misregulated microRNA (miRNA) expression. Histone acetylation and deacetylation are essential parts of gene regulation. The lysine residues in the N terminus and the surface of the nucleosome core (consists of 4 histone and DNA) are either acetylated or deacetylated during gene transcription. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) are the important families of catalytic enzymes that regulate transcription. HATs acetylate the e-amino group of lysine (K) residues on histones to neutralize the positive charge and create loosely coiled chromatin conformation to allow transcription. HDACs, on the other hand, remove the acetyl group from the histones, creating a tightly coiled, non-permissive chromatin conformation that in turn represses the transcription of genes. Depending on the target gene, chromatin structure alterations by both histone hyperacetylation and hypoacetylation can either propagate or suppress cancer progression. Stephanie Huang R, Cancer Epigenetics: Mechanisms and Crosstalk of a HDAC Inhibitor, Vorinostat.
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Last date updated on January, 2021