Endothelial infection with KSHV genes in vivo reveals that vGPCR initiates Kaposi's sarcomagenesis and can promote the tumorigenic potential of viral latent genes

Silvia Montaner, Akrit Sodhi, Alfredo Molinolo, Thomas H. Bugge, Earl T. Sawai, Yunsheng He, Yi Li, Patricio E. Ray, J. Silvio Gutkind

Research output: Contribution to journalArticlepeer-review

Abstract

The Kaposi's sarcoma herpesvirus (KSHV) has been identified as the etiologic agent of Kaposi's sarcoma (KS), but initial events leading to KS development remain unclear. Characterization of the KSHV genome reveals the presence of numerous potential oncogenes. To address their contribution to the initiation of the endothelial cell-derived KS tumor, we developed a novel transgenic mouse that enabled endothelial cell-specific infection in vivo using virus expressing candidate KSHV oncogenes. Here we show that transduction of one gene, vGPCR, was sufficient to induce angioproliferative tumors that strikingly resembled human KS. Endothelial cells expressing vGPCR were further able to promote tumor formation by cells expressing KSHV latent genes, suggestive of a cooperative role among viral genes in the promotion of Kaposi's sarcomagenesis.

Original languageEnglish (US)
Pages (from-to)23-36
Number of pages14
JournalCancer cell
Volume3
Issue number1
DOIs
StatePublished - Jan 2003
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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