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Kaposi's sarcoma

Coupling herpesvirus to angiogenesis

Nature volume 391, pages 24–25 (1998)Cite this article

Like experimentally mutated cellular GPCRs, KSHV-GPCR is fully active in the absence of chemokine ligands4. Bais et al.3 show that KSHV-GPCR can, indeed, act as a viral oncogene to transform NIH3T3 cells, and that this transformation is accompanied by secretion of VEGF. Spindle cells in Kaposi's sarcoma belong to the endothelial lineage, but they often express antigens characteristic of endothelial, macrophage and smooth-muscle cells. This indicates that they either represent pluripotent mesenchymal precursors, or are endothelial cells undergoing aberrant differentiation. KSHV DNA is present in most spindle cells, and also in endothelial cells and monocytes in Kaposi's sarcoma lesions.

The KSHV-GPCR gene is not the only viral oncogene to induce tumour formation and angiogenesis. Cells transformed by v-Ha-ras and v-raf (the constitutively active retroviral forms of cellular ras and raf) express increased VEGF5. But these genes induce a different signalling pathway from KSHV-GPCR. Bais et al. have found that GPCR triggers the JNK/SAPK and p38MAPK pathways, although they have not shown whether these cascades are involved in the induction of VEGF. So as many as three major signalling pathways that link membrane receptors with the nucleus in mammalian cells could, potentially, be involved in tumour progression by switching on angiogenesis. The viral interferon regulatory factor is another KSHV-encoded protein that can transform NIH3T3 cells and induce tumour formation in nude mice6.

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Figure 1: Kaposi's sarcoma biopsy.
Figure 2: ‘Oncogenic cluster’ in the genome of Kaposi's sarcoma-associated herpesvirus (KSHV).

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  1. the Chester Beatty Laboratories, Institute of Cancer Research, 237 Fulham Road, SW3 6JB, London, UK

    Chris Boshoff

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Boshoff, C. Coupling herpesvirus to angiogenesis. Nature 391, 24–25 (1998). https://doi.org/10.1038/34054

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