RNAs induced by Epstein-Barr virus nuclear antigen 2 in lymphoblastoid cell lines

Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1900-5. doi: 10.1073/pnas.0510612103. Epub 2006 Jan 30.

Abstract

Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) association with RBP-Jkappa is essential for regulation of virus and cell gene transcription and B lymphocyte transformation into infinitely proliferating lymphoblastoid cells (LCLs). To identify EBNA2-regulated cell genes in LCLs, an EBV recombinant that expresses EBNA2 with its C terminus fused in frame to a 4-hydroxytamoxifen (4HT)-dependent mutant estrogen receptor (E2HTF) was used to transform primary B lymphocytes to LCLs. In the presence of 4HT, E2HTF expression level and effects on the LMP1 promoter in transfected BJAB lymphoblasts were similar to EBNA2. In 4HT-supplemented medium, E2HTF EBV recombinant infected LCLs were also similar to EBNA2 LCLs in outgrowth but required higher serum and a restricted range of cell concentrations for consistent growth. In medium without 4HT, E2HTF localized to the cytoplasm, c-myc levels substantially decreased within 6 h, cells stopped growing, and levels of other EBNAs and LMP1 remained stable for 24 h. Over this 24-h period, 30 cell RNAs decreased 2-fold, and 51 other RNAs decreased 1.5-fold. These RNAs encode proteins important in cell adhesion or signaling, transcription, RNA processing, cell-cycle regulation, and survival. Real-time RT-PCR confirmed EBNA2-dependent expression of eight RNAs.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Cell Line
  • Cell Proliferation / drug effects
  • Computers
  • Epstein-Barr Virus Nuclear Antigens / metabolism*
  • Gene Expression Profiling
  • Gene Expression Regulation / drug effects
  • Herpesvirus 4, Human / genetics
  • Herpesvirus 4, Human / metabolism*
  • Humans
  • Lymphocytes / metabolism*
  • Lymphocytes / pathology*
  • Promoter Regions, Genetic / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • RNA / biosynthesis*
  • RNA / genetics*
  • Receptor, Notch1 / metabolism
  • Receptors, IgE / metabolism
  • Tamoxifen / analogs & derivatives
  • Tamoxifen / pharmacology

Substances

  • Epstein-Barr Virus Nuclear Antigens
  • Proto-Oncogene Proteins c-myc
  • Receptor, Notch1
  • Receptors, IgE
  • Tamoxifen
  • afimoxifene
  • RNA