Exosomes-secreted microRNAs play an important role in metastatic spread. During 
this process breast cancer cells acquire the ability to transmigrate through 
blood vessels by inducing changes in the endothelial barrier. We focused on 
miR-939 that is predicted to target VE-cadherin, a component of adherens 
junction involved in vessel permeability. By in silico analysis miR-939 was 
found highly expressed in the basal-like tumor subtypes and in our cohort of 63 
triple-negative breast cancers (TNBCs) its expression significantly interacted 
with lymph node status in predicting disease-free survival probability. We 
demonstrated, in vitro, that miR-939 directly targets VE-cadherin leading to an 
increase in HUVECs monolayer permeability. MDA-MB-231 cells transfected with a 
miR-939 mimic, released miR-939 in exosomes that, once internalized in 
endothelial cells, favored trans-endothelial migration of MDA-MB-231-GFP cells 
by the disruption of the endothelial barrier. Notably, when up taken in 
endothelial cells exosomes caused VE-cadherin down-regulation specifically 
through miR-939 as we demonstrated by inhibiting miR-939 expression in 
exosomes-releasing TNBC cells. Together, our data indentify an extracellular 
pro-tumorigenic role for tumor-derived, exosome-associated miR-939 that can 
explain its association with worse prognosis in TNBCs.