Epigenetic Regulation of Chromatin in Prostate Cancer

Abstract

Epigenetics refers to mitotically/meiotically heritable mechanisms that regulate gene transcription without a need for changes in the DNA code. Covalent modifications of DNA, in the form of methylation, and histone post-translational modifications, in the form of acetylation and methylation, constitute the epigenetic code of a cell. Both DNA and histone modifications are highly dynamic and often work in unison to define the epigenetic state of a cell. Most epigenetic mechanisms regulate gene transcription by affecting localized/genome-wide transitions between heterochromatin and euchromatin states, thereby altering the accessibility of the transcriptional machinery and in turn, reduce/increase transcriptional output. Altered chromatin structure is associated with cancer progression, and epigenetic plasticity primarily governs the resistance of cancer cells to therapeutic agents. In this chapter, we specifically focus on regulators of histone methylation and acetylation, the two well-studied chromatin post-translational modifications, in the context of prostate cancer.