SET domain and altered SET domain histone methyl transferases in cancer: A detailed insight

Abstract

Differential regulation of expression of gene is a determining factor in development of several genetic diseases and disorders, like cancer. Robust rearrangement of chromosome or genetic configuration and altered access of specific segments of genome are the definitive causes of unnatural cell proliferation. In the epigenetic model, the histone code hypothesis is represented by histone’s covalent chemical modifications and recruitment of several complexes at specified genome locations. Histone methylation is one epigenetic modification, involved in global or localized change in gene access, resulting in massive reconfiguration of gene expressional pathways to cause dis- eases and disorders. Altered methylation pattern of histones and alteration of structural and functional properties of histone methyl transferases are associated with several cancer induction, progression and differentiation. SET is a domain present in several histone methyl transferases and plays functional role in methylating specific lysine moieties in specific histones. Structural and functional alteration and deregulation of SET histone methyl transfe- rases have been shown to be causative of many types and stages of cancer. Altered SET histone methyl transfe- rases results in cancer by modulating structure of genome, transcriptional deregulation, altered recruitment of proteins, cross talking with other epigenetic modifications etc.