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Blood, 15 February 2002, Vol. 99, No. 4, pp. 1405-1410
NEOPLASIA
Cell surface proteoglycan syndecan-1 mediates hepatocyte growth
factor binding and promotes Met signaling in multiple myeloma
Patrick W. B. Derksen,
Robert M. J. Keehnen,
Ludo M. Evers,
Marinus H. J. van
Oers,
Marcel Spaargaren, and
Steven T. Pals
From the Department of Pathology and the Department of
Hematology, Academic Medical Center, University of Amsterdam, The
Netherlands.
Heparan sulfate proteoglycans (HSPGs) play a crucial role in growth
regulation by assembling signaling complexes and presenting growth
factors to their cognate receptors. Within the immune system, expression of the HSPG syndecan-1 (CD138) is characteristic of terminally differentiated B cells, ie, plasma cells, and their malignant counterpart, multiple myeloma (MM). This study explored the
hypothesis that syndecan-1 might promote growth factor signaling and
tumor growth in MM. For this purpose, the interaction was studied
between syndecan-1 and hepatocyte growth factor (HGF), a putative
paracrine and autocrine regulator of MM growth. The study demonstrates
that syndecan-1 is capable of binding HGF and that this growth factor
is indeed a potent stimulator of MM survival and proliferation.
Importantly, the interaction of HGF with heparan sulfate moieties on
syndecan-1 strongly promotes HGF-mediated signaling, resulting in
enhanced activation of Met, the receptor tyrosine kinase for HGF.
Moreover, HGF binding to syndecan-1 promotes activation of the
phosphatidylinositol 3-kinase/protein kinase B and
RAS/mitogen-activated protein kinase pathways, signaling routes that
have been implicated in the regulation of cell survival and
proliferation, respectively. These results identify syndecan-1 as a
functional coreceptor for HGF that promotes HGF/Met signaling in MM
cells, thus suggesting a novel function for syndecan-1 in MM tumorigenesis.
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