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Disruption of the intricate gene expression program represents one of major driving factors for the development, progression and maintenance of human cancer, and is often associated with acquired therapeutic resistance. At the molecular level, cancerous phenotypes are the outcome of cellular functions of critical genes, regulatory interactions of histones and chromatin remodeling complexes in response to dynamic and persistent upstream signals. A large body of genetic and biochemical evidence suggests that the chromatin remodelers integrate the extracellular and cytoplasmic signals to control gene activity. Consequently, widespread dysregulation of chromatin remodelers and the resulting inappropriate expression of regulatory genes, together, lead to oncogenesis. We summarize the recent developments and current state of the dysregulation of the chromatin remodeling components as the driving mechanism underlying the growth and progression of human tumors. Because chromatin remodelers, modifying enzymes and protein-protein interactions participate in interpreting the epigenetic code, selective chromatin remodelers and bromodomains have emerged as new frontiers for pharmacological intervention to develop future anti-cancer strategies to be used either as single-agent or in combination therapies with chemotherapeutics or radiotherapy.

Original publication

DOI

10.1038/onc.2015.513

Type

Journal article

Journal

Oncogene

Publication Date

25/08/2016

Volume

35

Pages

4423 - 4436

Keywords

Adenosine Triphosphatases, Animals, Carcinogenesis, Chromatin Assembly and Disassembly, Chromosomal Proteins, Non-Histone, DNA Helicases, Epigenomics, Humans, Mi-2 Nucleosome Remodeling and Deacetylase Complex, Neoplasms, Nuclear Proteins, Transcription Factors