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Epstein-Barr virus transcription activator Rta upregulates decoy receptor 3 expression by binding to its promoter

Cheng-Hsun Ho1, Chen-Fang Hsu, Pei-Fen Fong

  • 1Institute of Microbiology and Immunology, National Yang-Ming University, Number 155 Section 2 Linong Street, Taipei 112, Taiwan.

Journal of Virology
|February 16, 2007
PubMed

Insights

Epstein-Barr virus (EBV) reactivation enhances Decoy Receptor 3 (DcR3) expression. The EBV Rta protein directly binds the DcR3 promoter, upregulating its transcription, a process involving CREB-binding protein (CBP).

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Decoy receptor 3 (DcR3) is a soluble receptor overexpressed in cancers, promoting tumor survival and immune evasion.
  • DcR3 expression is linked to Epstein-Barr virus (EBV)-positive lymphomas, suggesting a role for EBV in its regulation.

Purpose of the Study:

  • To investigate the mechanism by which EBV influences DcR3 expression.
  • To identify the specific EBV components and cellular factors involved in DcR3 regulation.

Main Methods:

  • EBV reactivation in P3HR1 and 293 cells.
  • Analysis of DcR3 expression in EBV-infected cells, including those with deleted viral genes.
  • Reporter assays to assess promoter activity and transcription factor binding.
  • Western blotting and quantitative PCR to measure protein and gene expression.

Main Results:

  • EBV reactivation significantly enhanced DcR3 expression in infected cells.
  • Deletion of the EBV BRLF1 gene abolished this enhancement.
  • The EBV Rta protein directly binds to an Rta-responsive element (RRE) in the DcR3 promoter, driving transcription.
  • Co-expression of CREB-binding protein (CBP) potentiated Rta-mediated DcR3 upregulation.
  • The role of Rta-enhanced PI3-K activity in DcR3 expression was found to be minor.

Conclusions:

  • EBV Rta protein directly upregulates cellular DcR3 gene expression via binding to a specific RRE in its promoter.
  • This Rta-mediated transcriptional regulation is dependent on CBP, highlighting a novel mechanism of viral gene control.
  • These findings elucidate a direct link between EBV infection and the overexpression of a key cancer-associated decoy receptor.

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