Neuropilin-1 (Nrp1), originally characterized as an adhesion molecule in the nervous system, is a co-receptor for class-3
semaphorins.
Neuropilins and
semaphorins are highly expressed in a wide spectrum of
tumors and have been shown to influence their growth and vascularization. Despite the growing body of data on
neuropilin/
semaphorin regulation of
tumor growth, still the exact mechanism of their activity remains to be elucidated. Previously published data suggests that Nrp1 has both anti- and promigratory characteristics in different
tumor types, although no data is available on its role in
melanoma cells. In this paper, we studied the effect of Nrp1 downregulation on B16(F10)
melanoma cells migration. Our results show that the silencing of Nrp1 significantly increases the overall mobility of B16(F10) cells and changes their morphology. Moreover, Nrp1-silenced B16(F10) cells show a decreased response to
Sema3A. We also observed reduced binding of
Sema3A to these cells. Contrarily, no changes were observed in the binding of Sema3C to Nrp1-silenced B16(F10) cells, nor in its chemorepellent activity. Our results suggest that modulation of B16(F10) cells migratory ability by
semaphorin 3A can be preferentially mediated by Nrp1, while the contribution of
semaphorin 3C in this process is less evident. In addition, silencing of Nrp1 did not change the migratory ability of B16(F10) cells towards
VEGF.