| It has been proposed that solid tumor growth is angiogenesis dependent. Neovascularization in tumor may be a new target in cancer therapy. Thirty-five antiangiogenic therapies are currently being evaluated in clinical trials in nation cancer institute (NCI). Somatostatin (SS), as a neuroendocrine peptide, exerts a wide range physiological action. It not only inhibits neovascularization, also inhibits neovascularization. There are some studies that demonstrated differential expression of somatostatin receptor subtypes (SSTR) in human blood vessels and peritumoral veins. Currently available data suggest that somatostatin and its analogues might inhibit angiogenesis directly through somatostin receptors present on endothelial cells and indirectly through the inhibition of growth factors secretion such as vascular endothelial growth factor (VEGF) and reducing monocyte chemotaxis. In this experiment, we cultured cells obtained from healthy human umbilical cord vein, and indentified these cells according to the antigens expressed and their morphology by invert phase-contract microscope. With treatment of SS analogue octreotide , the human umbilical vein endothelial cell (HUVEC) growth inhibition, as assessed by MTT assay was observed. The increase in the number of cells in S phase by fluorescence activated flow cytometry analysis (FM). Interestingly, apoptosis was induced too. Using reverse transcription polymerasc chain reaction(RT-PCR), SSTR-3 were predominantly expressed , whereas SSTR-1 SSTR-2 ,SSTR-4 and SSTR-5 were undetectable in HUVEC . Because octreotide has high affinity for SSTR-2 and , to a lesser extent , SSTR-5 and SSTR-2 ,we concluded that octreotide antiproliferative effects may result from blockadeof mitogenic growth signal or induction of apoptosis following interaction with SSTR-3 . Endotheiial cell proliferation is the key step of angiogenesis, suggesting that octreotide may be an antitumor angiogenic compound directly affecting endothelial cells.
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