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Background  Disorganized angiogenesis is associated with several pathologies, including cancer. The identification of new genes that control tumor neovascularization can provide novel insights for future anti-cancer therapies.  Sprouty1 (SPRY1) , an inhibitor of the MAPK pathway, might be one of these new genes. We identified  SPRY1  by comparing the transcriptomes of untreated endothelial cells with those of endothelial cells treated by the angiostatic agent 16 K prolactin (16 K hPRL). In the present study, we aimed to explore the potential function of  SPRY1  in angiogenesis.    Results  We confirmed 16 K hPRL induced up-regulation of  SPRY1  in primary endothelial cells. In addition, we demonstrated the positive  SPRY1  regulation in a chimeric mouse model of human colon carcinoma in which 16 K hPRL treatment was shown to delay tumor growth. Expression profiling by qRT-PCR with species-specific primers revealed that induction of  SPRY1  expression by 16 K hPRL occurs only in the (murine) endothelial compartment and not in the (human) tumor compartment. The regulation of  SPRY1  expression was NF-κB dependent. Partial  SPRY1  knockdown by RNA interference protected endothelial cells from apoptosis as well as increased endothelial cell proliferation, migration, capillary network formation, and adhesion to extracellular matrix proteins.  SPRY1  knockdown was also shown to affect the expression of  cyclinD1  and  p21  both involved in cell-cycle regulation. These findings are discussed in relation to the role of SPRY1 as an inhibitor of ERK/MAPK signaling and to a possible explanation of its effect on cell proliferation.    Conclusions  Taken together, these results suggest that SPRY1 is an endogenous angiogenesis inhibitor.

Sprouty1, a new target of the angiostatic agent 16K prolactin, negatively regulates angiogenesis