Nature Genetics36, 687 - 693 (2004)
Published online: 27 June 2004; | doi:10.1038/ng1384
Kaposi sarcoma herpesvirus−induced cellular reprogramming contributes to the lymphatic endothelial gene expression in Kaposi sarcoma
Hsei-Wei Wang1, Matthew W B Trotter1, Dimitrios Lagos1, Dimitra Bourboulia1, Stephen Henderson1, Taija Mäkinen2, Stephen Elliman1, Adrienne M Flanagan3, Kari Alitalo2
& Chris Boshoff1
1
Cancer Research UK, Viral Oncology Group, Wolfson Institute for Biomedical Research, Cruciform Building, Gower Street, University College London, London WC1E 6BT, UK.
2
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Helsinki University Central Hospital, University of Helsinki, Finland.
3
Institute of Orthopaedics, University College London, UK.
The biology of Kaposi sarcoma is poorly understood because the dominant cell type in Kaposi sarcoma lesions is not known1,
2,
3,
4. We show by gene expression microarrays that neoplastic cells of Kaposi sarcoma are closely related to lymphatic endothelial cells (LECs) and that Kaposi sarcoma herpesvirus (KSHV)5,
6 infects both LECs and blood vascular endothelial cells (BECs) in vitro. The gene expression microarray profiles of infected LECs and BECs show that KSHV induces transcriptional reprogramming of both cell types. The lymphangiogenic molecules VEGF-D and angiopoietin-2 were elevated in the plasma of individuals with acquired immune deficiency syndrome and Kaposi sarcoma. These data show that the gene expression profile of Kaposi sarcoma resembles that of LECs, that KSHV induces a transcriptional drift in both LECs and BECs and that lymphangiogenic molecules are involved in the pathogenesis of Kaposi sarcoma.
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