KSHV activation of VEGF secretion and invasion for endothelial cells is mediated through viral upregulation of emmprin-induced signal transduction.

ABSTRACT: Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS)-one of the most common tumors arising in the setting of immune suppression. Hallmarks of KS lesions include KSHV-infected cells of endothelial lineage and neoangiogenesis. Promigratory factors secreted in the tumor microenvironment by KSHV-infected cells promote endothelial cell (EC) migration and angiogenesis but existing therapies targeting these pathways are not widely utilized. This underscores the need for additional characterization of KSHV-host interactions relevant to EC pathogenesis to identify new therapeutic targets. We recently demonstrated that de novo infection by KSHV promotes EC invasion through upregulation of extracellular matrix metalloproteinase inducer (emmprin)-a multifuncti

SUBMITTER: Dai L 

PROVIDER: S-EPMC3518925 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature