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Updated: Aug 14, 2025

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
Published on: September 14, 2010
The Kaposi's sarcoma progenitor enigma: KSHV-induced MEndT-EndMT axis
Julian Naipauer1, Enrique A Mesri2
1Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE), CONICET-Universidad de Buenos Aires, Buenos Aires, Argentina; Tumor Biology Program, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA; University of Miami- Center for AIDS Research (UM-CFAR)/Sylvester Comprehensive Cancer Center (CCC) Argentina Consortium for Research and Training in Virally Induced AIDS-Malignancies, University of Miami Miller School of Medicine, Miami, FL, USA; Miami Center for AIDS Research, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Abstract:
Endothelial-to-mesenchymal transition has been described in tumors as a source of mesenchymal stroma, while the reverse process has been proposed in tumor vasculogenesis and angiogenesis. A human oncogenic virus, Kaposi's sarcoma herpes virus (KSHV), can regulate both processes in order to transit through this transition 'boulevard' when infecting KS oncogenic progenitor cells. Endothelial or mesenchymal circulating progenitor cells can serve as KS oncogenic progenitors recruited by inflammatory cytokines because KSHV can reprogram one into the other through endothelial-to-mesenchymal and mesenchymal-to-endothelial transitions. Through these novel insights, the identity of the potential oncogenic progenitor of KS is revealed while gaining knowledge of the biology of the mesenchymal-endothelial differentiation axis and pointing to this axis as a therapeutic target in KS.
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