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Background The molecular mechanisms associated with the acquisition of a metastatic phenotype by melanoma cells are not very well understood. Therefore, the identification of molecular determinants involved in the metastatic switch that may either cause or contribute to the aggressiveness of melanoma is of primary relevance. We had previously identified neuropilin-1 (NRP-1), a co-receptor of the vascular endothelial growth factor-A (VEGF-A), as an important determinant of melanoma aggressiveness, in clones of the human melanoma cell line M14, expressing or not NRP-1 [1,2]. We demonstrated that even though the simultaneous presence of both VEGFR-2 and NRP-1 potentiates VEGF-A secretion and the aggressiveness of melanoma cells, NRP-1 is by itself able to promote cell invasion [1]. During melanoma progression, tumour cells show increased adhesiveness to the vascular wall, invade the extracellular matrix (ECM) and frequently form functional channels similar to vascular vessels (vasculogenic mimicry) [3]. In the present study we analysed the mechanisms responsible for the aggressive phenotype of NRP-1 expressing melanoma cells. Materials and methods Melanoma aggressiveness was evaluated in vitro as cell ability to migrate through an ECM layer in Boyden chambers and to form tubule-like structures on matrigel gels. Pre-incubation of the cells with specific blocking antibodies allowed the identification of specific integrins and other molecules relevant to these processes. The results obtained by anti-integrin antibodies, showing the involvement of avb 5i ntegrin in the aggressiveness of melanoma cells expressing NRP-1, were confirmed by ITGB5 gene silencing and by the use of cilengitide, a potent inhibitor of aν integrins activation. Results

Neuropilin-1 expressing melanoma cells as a model to study the aggressiveness of metastatic melanoma