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Blood, 15 December 2001, Vol. 98, No. 13, pp. 3717-3726
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Regulatory role of tetraspanin CD9 in tumor-endothelial cell
interaction during transendothelial invasion of melanoma cells
Natividad Longo,
María Yáñez-Mó,
María Mittelbrunn,
Gonzalo de la Rosa,
María-Luisa Muñoz,
Francisco Sánchez-Madrid, and
Paloma Sánchez-Mateos
From Servicio de Inmunología, Hospital General
Universitario Gregorio Marañón, and Servicio de
Inmunología, Hospital de la Princesa, Madrid, Spain.
Heterotypic interaction among tumor cells (TCs) and endothelial
cells (ECs) may play a critical role during the vascular dissemination of neoplastic cells and during pathologic angiogenesis in tumors. To
identify molecules involved in these processes, the distribution of
vascular junctional proteins was first studied by immunofluorescence at
sites of heterologous intercellular contact using TC-EC mosaic monolayers grown on 2-dimensional collagen. Several members of the
tetraspanin superfamily, including CD9, CD81, and CD151, were found to
localize at the TC-EC contact area. The localization of tetraspanins to
the TC-EC heterologous contact area was also observed during the active
transmigration of TCs across EC monolayers grown onto 3-dimensional
collagen matrices. Dynamic studies by time-lapse immunofluorescence
confocal microscopy showed an active redistribution of endothelial CD9
to points of melanoma insertion. Anti-CD9 monoclonal antibodies were
found to specifically inhibit the transendothelial migration of
melanoma cells; the inhibitory effect was likely caused by a
strengthening of CD9-mediated heterotypic interactions of TCs to the EC
monolayer. These data support a novel mechanism of tetraspanin-mediated
regulation of TC transcellular migration independent of TC motility and
growth during metastasis and a role for these molecules in the
formation of TC-EC mosaic monolayers during tumor angiogenesis.
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