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Retroviral oncogenes and TOR.

M Aoki1, P K Vogt

  • 1Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, BCC-239, La Jolla, CA 92037, USA.

Current Topics in Microbiology and Immunology
|October 17, 2003
PubMed
Summary

Certain retroviruses use PI 3-kinase and Akt as oncogenes, causing tumors. Their oncogenicity is blocked by rapamycin, an inhibitor of the target of rapamycin (TOR) kinase pathway, crucial for cell transformation.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • Retroviruses can act as oncogenes by incorporating PI 3-kinase and Akt.
  • These viral oncogenes induce tumors in vivo and transformation in vitro.

Purpose of the Study:

  • To investigate the role of the target of rapamycin (TOR) pathway in retroviral oncogenesis.
  • To determine the specificity of rapamycin's inhibitory effect on these oncogenic retroviruses.

Main Methods:

  • Utilized retroviral models expressing PI 3-kinase and Akt.
  • Assessed oncogenic transformation in cell culture and tumor formation in animals.
  • Tested the sensitivity of these viruses to rapamycin treatment.

Main Results:

  • Rapamycin specifically inhibited the oncogenicity of retroviruses utilizing PI 3-kinase/Akt.
  • Retroviruses with different oncogenes were insensitive to rapamycin.
  • Rapamycin targets the TOR kinase, affecting p70 S6 kinase and 4E-BP.

Conclusions:

  • The PI 3-kinase/Akt pathway's oncogenic transformation is dependent on TOR signaling.
  • TOR signaling to the translational machinery is essential for PI 3-kinase-driven oncogenesis.

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