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Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
Published on: November 8, 2011
The Epstein-Barr Virus Regulome in Lymphoblastoid Cells
Sizun Jiang1, Hufeng Zhou1, Jun Liang1
1Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Cell Host & Microbe
|October 13, 2017
Summary
Epstein-Barr virus (EBV) drives B cell transformation by altering 3D genome organization. This study maps the EBV regulome, revealing how viral elements control essential genes for cancer development.
Area of Science:
- Virology
- Cancer Biology
- Genomics
- Epigenetics
Background:
- Epstein-Barr virus (EBV) transforms B cells into lymphoblastoid cell lines (LCLs), serving as models for EBV-associated cancers.
- EBV nuclear antigens (EBNAs) and LMP1 are critical transcriptional regulators for LCL establishment, proliferation, and survival.
- Understanding the 3D genome organization is key to deciphering viral oncogenesis.
Purpose of the Study:
- To construct a comprehensive EBV regulome using LCL 3D genome organization maps.
- To identify viral and cellular genes and enhancers critical for EBV-driven B cell transformation.
- To elucidate the spatial regulation of key oncogenes and tumor suppressors by EBV.
Main Methods:
- 3D genome organization mapping in LCLs.
- Construction of a comprehensive EBV regulome (1,992 viral/cellular genes and enhancers).
- Functional deletion of EBNA2 sites and MYC super-enhancers (ESEs); EZH2 inhibition.
Main Results:
- Approximately 30% of LCL growth-essential genes were linked to EBV enhancers.
- Deletion of EBNA2 sites reduced target gene expression; EBV super-enhancers targeted MCL1, IRF4, and EBF.
- EBNA3A/3C altered CDKN2A/B spatial organization to suppress senescence; EZH2 inhibition reduced LCL growth.
Conclusions:
- This study provides a comprehensive spatial view of chromatin organization during EBV-driven cellular transformation.
- EBV utilizes 3D genome regulation to control host gene expression, promoting LCL proliferation and survival.
- Targeting EBV-mediated epigenetic modifications offers potential therapeutic strategies for EBV-associated cancers.
