Abstract
The chromatin remodeling complexes alter chromatin structures. They remodel nucleosomes in ATP-dependent manner and have essential roles in DNA damage repair, recombination, replication and transcriptional control. Increasing evidences indicate that subunits of chromatin remodelers are mutated and/or deregulated in a number of human cancers, and how they influence the cancer gene expression program during cancer initiation and progression is becomming clearer. Therefore, chromatin remodeling complexes arose as promising new targets for the treatment of human cancers. In this review, chromatin remodeling complexes, their epigenetic reader domains and available inhibitors are described. The insights into the misregulated chromatin remodelers pathways in human malignancies and the novel approach targeting deregulated chromatin remodelers to improve chemotherapy efficiency are discussed.
Highlights
Malignant cell abuses chromatin remodelers in different waysTo meet the demands of growth, cancer cells reprogram their metabolism
A nucleosome is a basic unit of DNA packaging in humans, consisting of 146 bp DNA wrapped around a histone octamer
The complexity and specificity of chromatin remodeling complexes is achieved by their accessory subunits, that contain additional epigenetic reader domains, RNA binding domains or even form complexes with histone deacethylases (HDAC) and histone methyltransferases (HMT)[2]
Summary
To meet the demands of growth, cancer cells reprogram their metabolism. The connection between cancer and chromatin remodelers arose two decades ago, when SNF5 gene, which encodes a member of the chromatinremodelling SWI/SNF complex, was found to be mutated in malignant rhabdoid tumours[4]. Evidence has been accumulating how the deregulated chromatin remodelers can support the uncontrolled growth of the cell
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