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Background  Shb is a signaling protein downstream of vascular endothelial growth factor receptor-2 and  Shb  deficiency has been found to restrict tumor angiogenesis. The present study was performed in order to assess metastasis in  Shb  deficiency using B16F10 melanoma cells.    Methods  B16F10 melanoma cells were inoculated subcutaneously on wild type or  Shb  +/− mice. Primary tumors were resected and lung metastasis determined after tumor relapse. Lung metastasis was also assessed after bone marrow transplantation of wild type bone marrow to  Shb  +/− recipients and  Shb  +/− bone marrow to wild type recipients. Primary tumors were subject to immunofluorescence staining for CD31, VE-cadherin, desmin and CD8, RNA isolation and isolation of vascular fragments for further RNA isolation. RNA was used for real-time RT-PCR and microarray analysis.    Results  Numbers of lung metastases were increased in  Shb  +/− or −/− mice and this coincided with reduced pericyte coverage and increased vascular permeability. Gene expression profiling of vascular fragments isolated from primary tumors and total tumor RNA revealed decreased expression of different markers for cytotoxic T cells in tumors grown on  Shb  +/− mice, suggesting that vascular aberrations caused altered immune responses.    Conclusions  It is concluded that a unique combinatorial response of increased vascular permeability and reduced recruitment of cytotoxic CD8+ cells occurs as a consequence of  Shb  deficiency in B16F10 melanomas. These changes may promote tumor cell intravasation and metastasis.    Electronic supplementary material  The online version of this article (doi:10.1186/s12885-015-1269-y) contains supplementary material, which is available to authorized users.

Vascular dysfunction and increased metastasis of B16F10 melanomas in Shb deficient mice as compared with their wild type counterparts