Somatostatin and its analogs are active in the inhibition of SST receptor-p
ositive endocrine neoplasms, but their activity and mechanism in non endocr
ine tumors is not clear. Somatostatin potently inhibited growth of a Kaposi
's sarcoma xenograft in nude mice, yet in vitro the tumor cells did not exp
ress any known somatostatin receptors and were not growth inhibited by soma
tostatin. Histological examination revealed limited vascularization in the
somatostatin-treated tumors as compared with the controls. Somatostatin was
a potent inhibitor of angiogenesis in an in vivo assay. In vitro, somatost
atin inhibited endothelial cell growth and invasion. Migration of monocytes
, important mediators of the angiogenic cascade, was also inhibited by soma
tostatin. Both cells types expressed somatostatin receptor mRNAs. These dat
a demonstrate that somatostatin is a potent antitumor angiogenesis compound
directly affecting both endothelial and monocytic cells. The debated funct
ion of somatostatin in tumor treatment and the design of therapeutic protoc
ols should be reexamined considering these data.