BORIS promotes chromatin regulatory interactions in treatment-resistant cancer cells.

ABSTRACT: The CCCTC-binding factor (CTCF), which anchors DNA loops that organize the genome into structural domains, has a central role in gene control by facilitating or constraining interactions between genes and their regulatory elements^1,2. In cancer cells, the disruption of CTCF binding at specific loci by somatic mutation^3,4 or DNA hypermethylation⁵ results in the loss of loop anchors and consequent activation of oncogenes. By contrast, the germ-cell-specific paralogue of CTCF, BORIS (brother of the regulator of imprinted sites, also known as CTCFL)⁶, is overexpressed in several cancers^7-9, but its contributions to the malignant phenotype remain unclear. Here we show that aberrant upregulation of BORIS promotes chromatin interactions in AL

SUBMITTER: Debruyne DN 

PROVIDER: S-EPMC7010522 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature