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

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.