Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 113, Issue 49, Pages 14121-14126Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1616697113
Keywords
Epstein-Barr virus; super-enhancer; eRNA; MYC
Categories
Funding
- National Cancer Institute (NCI) [R01CA047006, R01CA170023, R01CA085180]
- National Institute of Allergy and Infectious Diseases [R01AI123420]
- NCI [R01CA082036]
- National Institute of Dental and Craniofacial Research [R01DE025208, R01DE024971]
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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.
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