Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, 2300 Eye Street, N.W., Washington, DC 20037, USA
Both the development and progression of cancerous phenotypes are driven by dysfunctional regulatory gene products, at-least, in-part. The resulting deregulatory processes are result of the genomic, epigenomic and gene expression machineries in cancer cells – all translating into changes in appropriate gene expression programs. At the molecular level, the process of gene expression in cancer cells is regula ted by epigenomic interactions of chromatin remodelers, bromodomain-containing proteins, and histones in the context of target gene chromatin. Therefore, any dysfunction of genes for chromatin remodeling proteins and chromatin-interacting proteins with bromodomains may inappropriately alter the steady state levels of regulatory genes with roles in oncogenesis. Recent advances in cancer epigenetic re-emphasize the significance of studying epigenomic regulation of gene expression for identifying the next generation of cancer therapeutic targets. Consistent with this notion, there is a widespread dysregulation of chromatin remodeling and bromodomain-containing proteins in human cancer. Hence, specific chromatin remodeling factors and/or bromodomain-containing proteins have emerged as promising candidates for the development of anti-cancer therapeutics either alone or as a part of combination therapy. The lecture will provide an overview of the current status and approaches to target such molecules with a hope to develop superior anti-cancer agents.