| Literature DB >> 27864512 |
Jun Liang1,2, Hufeng Zhou1,2, Catherine Gerdt1, Min Tan1, Tyler Colson1, Kenneth M Kaye1, Elliott Kieff3,2, Bo Zhao3.
Abstract
Epstein-Barr virus (EBV) super-enhancers (ESEs) are essential for lymphoblastoid cell (LCL) growth and survival. Reanalyses of LCL global run-on sequencing (Gro-seq) data found abundant enhancer RNAs (eRNAs) being transcribed at ESEs. Inactivation of ESE components, EBV nuclear antigen 2 (EBNA2) and bromodomain-containing protein 4 (BRD4), significantly decreased eRNAs at ESEs -428 and -525 kb upstream of the MYC oncogene transcription start site (TSS). shRNA knockdown of the MYC -428 and -525 ESE eRNA caused LCL growth arrest and reduced cell growth. Furthermore, MYC ESE eRNA knockdown also significantly reduced MYC expression, ESE H3K27ac signals, and MYC ESEs looping to MYC TSS. These data indicate that ESE eRNAs strongly affect cell gene expression and enable LCL growth.Entities:
Keywords: Epstein–Barr virus; MYC; eRNA; super-enhancer
Mesh:
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Year: 2016 PMID: 27864512 PMCID: PMC5150416 DOI: 10.1073/pnas.1616697113
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205