Histone Acetylation / Deacetylation and Cancer: An “Open” and “Shut” Case?

S.   G.   Gray; B.   T.   Teh

Abstract

DNA in eukaryotic cells is packaged into chromatin. The main packaging component of chromatin is the nucleosome, and this is composed of proteins known as histones. Histones can be reversibly modified in several ways, and the best characterized of these modifications is histone acetylation. This is a reversible modification, which is carried out by two families of enzymes, the histone acetyltransferases (HATs), and the histone deacetylases (HDACs). These enzymes have important activities in many cellular processes including transcription, DNA replication and cell cycle progression. The mechanisms underlying tumor formation are multifaceted, and often involve mutations or alterations of genes involved with the regulation and control of the cell cycle or cell death. Because of their important roles in the regulation of such events, enzymes that affect histone acetylation status are increasingly being associated with tumors. This article describes some of the current knowledge about histone acetyltransferases and histone deacetylases, and how their multitudinal roles in cellular events may have important roles in tumorigensis.

Keywords: Histone Acetylation/, histone acetyltransferases, GNAT (GCN5-related N-acetyltransferase), TUMORIGENESIS, Oncogenes, Tumor Suppressor Genes, DNA Repairing Genes, Methylation, CELLULAR PROCESSES, Retinoblastoma Protein