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The EBNA-3 gene family proteins disrupt the G2/M checkpoint

Kenia G Krauer1, Andrew Burgess, Marion Buck

  • 1Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Brisbane, Australia. keniaK@qimr.edu.au

Oncogene
|January 13, 2004
PubMed

Insights

Epstein-Barr nuclear antigens (EBNA)-3, -4, and -6 disrupt the G2/M cell cycle checkpoint, increasing cell death from certain drugs. This suggests a novel role for these EBNA proteins in manipulating host cell cycle processes.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Epstein-Barr nuclear antigens (EBNA) are viral proteins crucial for EBV-driven lymphoproliferation.
  • EBNA-3, -4, and -6 were known transcriptional regulators.
  • The role of these EBNA proteins in cell cycle regulation was previously unexplored.

Purpose of the Study:

  • To investigate the function of EBNA-3, -4, and -6 proteins beyond transcriptional regulation.
  • To determine if these EBNA proteins impact the G2/M cell cycle checkpoint.

Main Methods:

  • Lymphoblastoid cell lines (LCLs) were treated with G2/M initiating drugs like azelaic bishydroxamine (ABHA).
  • Cell cycle analysis was performed to assess checkpoint responses.
  • Individual expression of EBNA proteins was evaluated for effects on cell cycle disruption.

Main Results:

  • EBNA-3, -4, and -6 expression disrupted the G2/M checkpoint response to ABHA, leading to increased cell death.
  • EBNA-3 family proteins also disrupted G2/M checkpoints induced by etoposide and hydroxyurea.
  • EBNA-2 and EBNA-5 did not exhibit these G2/M checkpoint disrupting effects.

Conclusions:

  • EBNA-3, -4, and -6 proteins possess a novel function in disrupting the host cell G2/M checkpoint.
  • These EBNA proteins may interfere with ATM/ATR signaling pathways involved in checkpoint control.
  • The findings reveal a more complex role for EBNA-3, -4, and -6 in manipulating host cell machinery.

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