IMR Press / FBL / Volume 13 / Issue 3 / DOI: 10.2741/2722

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Molecular mechanisms of the antiproliferative activity of somatostatin receptors (SSTRs) in neuroendocrine tumors
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1 Laboratory of Pharmacology, Department of Oncology, Biology and Genetics, University of Genova, viale Benedetto XV, 2, 16132 Genova, Italy
Front. Biosci. (Landmark Ed) 2008, 13(3), 822–840;
Published: 1 January 2008

The current treatment of neuroendocrine tumors include the use of somatostatin (SST) agonists. These compounds are able to control most of the symptoms caused by the hypersecretory activity of the tumor cells, and for this reason, they provide a significant improvement in the well-being of the patients. Although, several reports also showed a possible direct antiproliferative activity of SST agonists in different neuroendocrine tumors, the therapeutic potential of an in vivo antiproliferative activity mediated by SST receptors is still debated. In recent years, there has been great insights on understanding the molecular basis of the antitumoral activity of SST that appears to be exerted via both direct and indirect mechanisms. Direct mechanisms require the activation of SST receptors in tumor cells and the induction of cell cycle arrest or apoptosis, mainly through the regulation of phosphotyrosine phosphatase (PTP) and MAP kinase activities. The indirect mechanisms involve the inhibition of tumor angiogenesis and the inhibition of the secretion of factors which are required for tumor growth. Here, we will review the molecular mechanisms which are implicated in the antiproliferative activity of SST. Such an understanding is necessary for improving the antitumoral efficacy of SSTR agonists as well as for the development of novel therapeutic strategies.

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