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p53 in polyoma virus transformed REF52 cells

O Mor1, M Read, M Fried

  • 1Eukaryotic Gene Organisation and Expression Laboratory, Imperial Cancer Research Fund, London.

Oncogene
|January 28, 1998
PubMed
Summary
This summary is machine-generated.

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Polyoma virus (Py) middle T-antigen (PyMT) transforms cells lacking functional p53, unlike other DNA tumor viruses. PyMT oncogene mediates transformation by bypassing p53

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Small DNA tumor viruses typically target the p53 tumor suppressor gene product.
  • Polyoma virus (Py) T antigens have not been previously observed to interact with p53.

Purpose of the Study:

  • To investigate the mechanism of cellular transformation by Polyoma virus (Py) middle T-antigen (PyMT).
  • To determine the role of the p53 tumor suppressor gene in PyMT-mediated transformation.

Main Methods:

  • Transformation assays using primary mouse embryo fibroblasts, REF52 cells, and their p53-deficient counterparts.
  • Western blot analysis to detect p53 protein accumulation and p53-induced proteins (p21/WAF1, MDM2).
  • Cell cycle analysis following DNA damage (X-irradiation) to assess G1/S and G2/M blocks.

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Main Results:

  • PyMT alone transforms rodent cells lacking functional p53, but not normal cells without co-operating oncogenes.
  • Py-transformed cells (Py-REF52) show no significant p53 accumulation, unlike SV40-transformed cells (SV-REF52).
  • Py-REF52 cells exhibit a G1/S cell cycle block after X-irradiation, but not a G2/M block, indicating functional p53 transactivation of DNA damage response.

Conclusions:

  • Polyoma virus (Py) does not interfere with DNA damage-induced p53 transactivation, differing from most DNA tumor viruses.
  • Absence of functional p53 facilitates transformation by the PyMT oncogene, even without cooperating oncogenes.
  • PyMT-mediated transformation may involve mechanisms distinct from p53 inhibition, potentially bypassing p53-dependent cell cycle checkpoints.