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PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the

P Wimmer1, J Berscheminski1, P Blanchette2

  • 1Department of Viral Transformation, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.

Oncogene
|March 17, 2015
PubMed

Insights

The E1B-55K viral oncoprotein

Area of Science:

  • Oncogenic mechanisms
  • Viral oncogenesis
  • Cellular transformation

Background:

  • Cellular tumor suppressor p53 modulation is key in E1A/E1B-55K tumorigenesis.
  • Promyelocytic leukemia nuclear body (PML-NB)/PML oncogenic domain (POD) factors contribute to cell transformation.
  • Biochemical consequences of E1B-55K interaction with SUMO-dependent PML-IV and PML-V remain unclear.

Purpose of the Study:

  • To investigate the role of E1B-55K/PML interaction in tumorigenesis.
  • To elucidate the biochemical consequences of SUMO-dependent PML-IV and PML-V interaction with E1B-55K.
  • To define the PML interaction motif within E1B-55K.

Main Methods:

  • Mutational analysis of E1B-55K to define PML interaction motif.
  • Assessment of E1B-55K binding to PML.
  • Evaluation of E1B-55K's effect on p53 SUMOylation and transactivation.
  • Testing the oncogenic transformation potential of E1B-55K mutants.

Main Results:

  • E1B-55K/PML binding is not essential for interaction with p53, Mre11, or Daxx.
  • E1B-55K mutants deficient in PML localization lost the ability to SUMOylate p53.
  • These mutants also failed to inhibit p53 transactivation and efficiently transform cells.
  • E1B-55K-dependent p53 SUMOylation is crucial for efficient cell transformation.

Conclusions:

  • E1B-55K's SUMO ligase activity is intrinsically linked to its growth-promoting oncogenic functions.
  • PML localization is critical for E1B-55K's oncogenic activities.
  • The study highlights the importance of PML-NB integrity in viral oncogenesis.

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