Abstract
Epigenetic regulation refers to alterations to the chromatin template that collectively establish differential patterns of gene transcription. Post-translational modifications of the histones play a key role in epigenetic regulation of gene transcription. In this review, we provide an overview of recent studies on the role of histone modifications in carcinogenesis. Since tumour-selective ligands such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are well-considered as promising anti-tumour therapies, we summarise strategies for improving TRAIL sensitivity by inhibiting aberrant histone modifications in cancers. In this perspective we also discuss new epigenetic drug targets for enhancing TRAIL-mediated apoptosis.
Highlights
In humans, the genetic information (DNA) is contained in 23 chromosome pairs
Since epigenetics plays a crucial role in DNAbased processes, histone modifications are very important in cell growth in normal and disease states such as carcinogenesis
We provide an overview of post-translational modifications of histones and the enzymes involved in the addition or removal of these modifications
Summary
The genetic information (DNA) is contained in 23 chromosome pairs. These chromosomes are composed of DNA and histone proteins that form highly condensed chromatin. Acetylation is related to increased gene transcription, while deacetylation is connected to repression of gene transcription [Figure 1] This dynamic process is catalysed by three groups of enzymes: (1) histone acetyltransferases (HATs), known as “writers”, are responsible for transferring acetyl groups to targeted lysine residues; (2) histone deacetylases (HDACs), known as “erasers”, are found to remove acetyl groups; and (3) bromodomain proteins, known as “readers”, recognize acetylated lysine residues. Besides the aforementioned methylation and acetylation, other types of post-translational modifications are identified on histones, such as lysine ubiquitinoylation, sumoylation and ADP-ribosylation These modifications are mostly reported to relate to DNA damage and repair. PRMT5 1 Relapsed/refractory B cell non-Hodgkin methylation lymphoma (NHL) or advanced solid tumours
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