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J Biol Chem, Vol. 274, Issue 39, 27617-27622, September 24, 1999
,, and
From the Institute for Cancer Research and Treatment (I.R.C.C.) and
Department of Genetics, Biology, and Biochemistry, University of Torino
Medical School, 10060 Candiolo, Italy, the § Department of
Biomedical Sciences and Oncology, University of Torino Medical School,
10100 Torino, Italy, the ¶ National Institute for Cancer Research
and Center of Advanced Biotechnology, 16100 Genova, Italy, and the
Recent evidence suggesting vascular
endothelial growth factor-C (VEGF-C), which is a regulator of lymphatic
and vascular endothelial development, raised the question whether this
molecule could be involved in Kaposi's sarcoma (KS), a strongly
angiogenic and inflammatory tumor often associated with infection by
human immunodeficiency virus-1. This disease is characterized by the
presence of a core constituted of three main populations of
"spindle" cells, having the features of lymphatic/vascular
endothelial cells, macrophagic/dendritic cells, and of a mixed
macrophage-endothelial phenotype.
In this study we evaluated the biological response of KS cells to
VEGF-C, using an immortal cell line derived from a KS lesion (KS IMM),
which retains most features of the parental tumor and can induce
KS-like sarcomas when injected subcutaneously in nude mice. We show
that VEGFR-3, the specific receptor for VEGF-C, is expressed by KS IMM
cells grown in vitro and in vivo. In vitro, VEGF-C induces the tyrosine phosphorylation of VEGFR-2, a receptor also
for VEGF-A, as well as that of VEGFR-3. The activation of these two
receptors in KS IMM cells is followed by a dose-responsive mitogenic
and motogenic response. The stimulation of KS IMM cells with a mutant
VEGF-C unable to bind and activate VEFGR-2 resulted in no proliferative
response and in a weak motogenic stimulation, suggesting that VEGFR-2
is essential in transducing a proliferative signal and cooperates with
VEGFR-3 in inducing cell migration.
Our data add new insights on the pathogenesis of KS, suggesting that
the involvement of endothelial growth factors may not only determine
KS-associated angiogenesis, but also play a critical role in
controlling KS cell growth and/or migration and invasion.
Molecular/Cancer Biology Laboratory, Haartman Institute,
University of Helsinki, SF-00014 Helsinki, Finland
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