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Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism. | LitMetric

Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism.

Cell Rep

Whitehead Institute for Biomedical Research, 455 Main Street, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. Electronic address:

Published: April 2018

AI Article Synopsis

Article Abstract

Transcriptional dysregulation of the MYC oncogene is among the most frequent events in aggressive tumor cells, and this is generally accomplished by acquisition of a super-enhancer somewhere within the 2.8 Mb TAD where MYC resides. We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5929158PMC
http://dx.doi.org/10.1016/j.celrep.2018.03.056DOI Listing

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