David N Debruyne, Ruben Dries, Satyaki Sengupta, Davide Seruggia, Yang Gao, Bandana Sharma, Hao Huang, Lisa Moreau, Michael McLane, Daniel S Day, Eugenio Marco, Ting Chen, Nathanael S Gray, Kwok-Kin Wong, Stuart H Orkin, Guo-Cheng Yuan, Richard A Young, Rani E George
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 elements1,2 . In cancer cells, the disruption of CTCF binding at specific loci by somatic mutation3,4 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 cancers7-9 , but its contributions to the malignant phenotype remain unclear...
August 7, 2019: Nature