Related Experiment Video
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.
Kaposi's sarcoma herpes virus (KSHV) drives endothelial-to-mesenchymal transition in progenitor cells, revealing a key mechanism in cancer development and a potential therapeutic target.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- Endothelial-to-mesenchymal transition (EndMT) contributes to tumor stroma.
- Mesenchymal-to-endothelial transition (MEnT) is implicated in tumor angiogenesis.
- Kaposi's sarcoma herpes virus (KSHV) is an oncogenic human virus.
Purpose of the Study:
- To elucidate the role of KSHV in regulating EndMT and MEnT.
- To identify the oncogenic progenitor cells in Kaposi's sarcoma (KS).
- To explore the mesenchymal-endothelial differentiation axis as a therapeutic target.
Main Methods:
- Analysis of KSHV's influence on endothelial and mesenchymal progenitor cells.
- Investigation of cellular reprogramming by KSHV during infection.
- Study of inflammatory cytokine recruitment of progenitor cells.
Main Results:
- KSHV actively regulates both EndMT and MEnT in infected progenitor cells.
- KSHV can reprogram endothelial progenitor cells into mesenchymal progenitor cells and vice versa.
- This reprogramming facilitates the transition 'boulevard' crucial for KS oncogenesis.
Conclusions:
- The study identifies circulating endothelial or mesenchymal progenitor cells as potential KS oncogenic progenitors.
- KSHV-mediated reprogramming along the mesenchymal-endothelial differentiation axis is central to KS development.
- Targeting this axis presents a novel therapeutic strategy for Kaposi's sarcoma.
More Related Videos
Related Concept Videos
Mechanisms of Retrovirus-induced Cancers
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Abnormal Proliferation
Immunodeficiency Diseases
There are three main causes of immunodeficiency...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...

