Role of Somatostatin Receptor in Pancreatic Neuroendocrine Tumor Development, Diagnosis, and Therapy

Abstract

Pancreatic neuroendocrine tumors (pNETs) are rare and part of the diverse family of neuroendocrine neoplasms (NENs). Somatostatin receptors (SSTRs), which are widely expressed in NENs, are G-protein coupled receptors that can be activated by somatostatins or its synthetic analogs. Therefore, SSTRs have been widely researched as a diagnostic marker and therapeutic target in pNETs. A large number of studies have demonstrated the clinical significance of SSTRs in pNETs. In this review, relevant literature has been appraised to summarize the most recent empirical evidence addressing the clinical significance of SSTRs in pNETs. Overall, these studies have shown that SSTRs have great value in the diagnosis, treatment, and prognostic prediction of pNETs; however, further research is still necessary.

Potential Targets Other Than PSMA for Prostate Cancer Theranostics: A Systematic Review

“…Somatostatin receptors (SSTRs) are a group of 5 subtype G protein-coupled transmembrane receptors that have a role in growth hormone, insulin and glucagon secretion, and in neuronal activity [ 65 ]. They are usually overexpressed in neuroendocrine tumors [ 65 ].…”

“…Somatostatin receptors (SSTRs) are a group of 5 subtype G protein-coupled transmembrane receptors that have a role in growth hormone, insulin and glucagon secretion, and in neuronal activity [ 65 ]. They are usually overexpressed in neuroendocrine tumors [ 65 ]. SSTRs have a low expression in the normal prostate, even if it increases with patient age and in hypertrophic and hyperplastic prostate [ 45 ].…”

Somatostatin and Its Receptor System in Colorectal Cancer

“…The SRIF signal pathways are well described in the literature [ 16 ], prompting the author to attempt to provide a different scope of information. However, it is worth highlighting that the main pathways regulated by the activation of SST1–5 lead to the inhibition of secretion (e.g., other neuropeptides, hormones, growth factors, and cytokines), cell proliferation, migration, and angiogenesis [ 12 , 16 , 27 , 100 , 106 , 107 ] ( Table 1 ).…”

“…Upon binding to SST, intracellular pathways are activated by SST1–5, leading to antiproliferative and anti-secretory effects. In addition, activation of SST2 and SST3 also exerts pro-apoptotic effects [ 106 , 107 ]. Recent studies on human brain extracts indicate that SST binds primarily to several members of the P-type ATPase family.…”

“…Two subfamilies of SST receptors have been described on the basis of chemical structure identity and pharmacological characteristics: the first class, comprising SST2, SST3, and SST5, binds synthetic SST analogues (SAAs), such as octreotide (OCT) and lanreotide, while the second-class receptors, SST1 and SST4, do not interact with these agonists [ 113 ]. The basic signaling pathways in the action of SST are also known, ultimately exerting anti-secretory, anti-proliferative, and pro-apoptotic effects (via SST2 and SST3) [ 12 , 107 ].…”