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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)

Published on: September 14, 2010

PI3Kγ mediates kaposi's sarcoma-associated herpesvirus vGPCR-induced sarcomagenesis

Daniel Martin1, Rebeca Galisteo, Alfredo A Molinolo

  • 1Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.

Cancer Cell
|June 14, 2011
PubMed

Insights

Rapamycin effectively treats Kaposi

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV) induces angioproliferative tumors.
  • mTOR inhibitors like rapamycin show clinical activity against KSHV-induced tumors.
  • Prolonged mTOR inhibition poses risks for immunocompromised patients, such as those with AIDS-Kaposi's sarcoma (KS).

Purpose of the Study:

  • To investigate cell type-specific signaling pathways used by KSHV oncogenes to activate mTOR.
  • To identify therapeutic targets for halting KS development with minimal immune suppression.

Main Methods:

  • Explored KSHV oncogene signaling pathways.
  • Utilized an endothelial-specific gene delivery system to model KS development.
  • Employed genetic and pharmacological approaches to target PI3Kγ.

Main Results:

  • PI3Kγ (phosphatidylinositol 3-kinase gamma) is essential for vGPCR oncogene signaling to Akt/mTOR.
  • PI3Kγ exhibits restricted tissue distribution, suggesting a cell type-specific role.
  • Targeting PI3Kγ effectively halts KS development in a relevant model.

Conclusions:

  • KSHV oncogenes utilize PI3Kγ for mTOR activation in a cell type-specific manner.
  • PI3Kγ is a potential therapeutic target for KS, offering a strategy to minimize immune suppression.
  • Targeting PI3Kγ may provide a safer alternative to broad mTOR inhibition in immunocompromised patients.

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