Somatostatin receptor biology in neuroendocrine and pituitary tumours: part 2--clinical implications.

摘要

In part 1 of our review on somatostatin (SST) receptor biology in neuroendocrine tumours, the somatostatin receptor (SSTR) as a G-protein coupled receptor (GPCR), and the anti-tumour effects of SST and SSTR post-signalling pathways, were reviewed. To recapitulate, SST is a peptide hormone which acts mainly as an inhibitor in many endocrine systems. SST has five receptor subtypes (SSTR1-5) with SSTR2 as the most commonly expressed form in both normal and tumoral tissues. SST has been widely investigated for its anti-tumoral effects and their mechanisms, and currently there are two SST analogues (lanreotide and octreotide) in clinical use. The anti-proliferative action of SST mainly occurs through phosphotyrosine phosphatases which modulate MAPK and PI3K/Akt pathways. On the other hand, its anti-secretory action occurs through decreased intracellular cAMP, K+ and Ca++ levels. While part 1 of our review has principally focused on the molecular components of SST action, part 2 will cover the clinical implications of these molecular effects, starting from SSTR subtype tissue distribution and SST analogue use in the diagnosis and treatment of neuroendocrine tumours.