Somatostatin inhibits PDGF‐stimulated Ras activation in human neuroblastoma cells

FEBS Letters

Vicentini, Lucia M.¹  Scita, Giorgio²  Cattaneo, Maria Grazia¹ 

[1] Department of Pharmacology, University of Milano, Via Vanvitelli, 32, 20129 Milano, Italy;European Institute of Oncology, Via Ripamonti, 435, Milano, Italy

关键词: Somatostatin;    Human neuroblastoma;    Ras activation;    PDGF receptor phosphorylation;    SST;    somatostatin;    PDGF;    platelet-derived growth factor;    MAP kinase;    mitogen-activated protein kinase;    PTx;    pertussis toxin;    GAP;    GTPase activating protein;   

DOI  :  10.1016/S0014-5793(99)01218-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The main physiological role of somatostatin (SST) is the control of hormone secretion. Recently, SST has been shown to exert antiproliferative effects on some human tumors via both direct and indirect mechanisms. We have previously found that in the human neuroblastoma cell line SY5Y the SST analogue lanreotide (BIM 23014) inhibited serum-stimulated cell proliferation and MAP kinase activity. Here, we examine the effect of SST on PDGF-induced Ras activation. We found that SST suppressed PDGF-induced Ras activation in a pertussis toxin (PTx)-independent and peroxovanadate-dependent manner. Ras-specific GTPase activating protein (GAP) activities were not altered by SST treatment. On the contrary, PDGF-induced PDGF receptor phosphorylation was decreased by SST in a PTx-independent, peroxovanadate-dependent manner, likely accounting for the SST-mediated inhibition of PDGF-induced Ras activation.

【 授权许可】

Unknown