We further identify and characterize the mechanism by which tumor-derived EVs circumvent the low physiologic rate of transcytosis in the BBB by decreasing the brain endothelial expression of rab7 and increasing the efficiency of their transport.
Rab7 inhibition reversed <i>lal</i><sup>-/-</sup> EC dysfunctions, including decreasing their enhanced migration and permeability of tumor-stimulatory myeloid cells, and suppressed EC-mediated stimulation of <i>in vitro</i> tumor cell transmigration, proliferation, and migration and <i>in vivo</i> tumor growth and metastasis.
Combination between SAHA and Simvastatin could also significantly decrease the tumor growth in xenografted mice by inducing apoptosis and inhibiting Rab7 prenylation.