Ask about this productRelated genes to: SSTR5 Blocking Peptide
- Gene:
- SSTR5 NIH gene
- Name:
- somatostatin receptor 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-12
- Date modifiied:
- 2015-08-26
Related products to: SSTR5 Blocking Peptide
Related articles to: SSTR5 Blocking Peptide
- Somatotropinomas are a subtype of pituitary adenomas that have a particular predilection to invade the cavernous sinus. The objective of this systematic review was to examine the evidence regarding the molecular basis for cavernous sinus invasion in somatotropinomas. This review was conducted in accordance with the 2020 PRISMA guidelines on the 13th of April 2025. Inclusion criteria were reports of associations between somatotropinoma molecular changes and cavernous sinus invasion in adult patients. Title/abstract screening and full text screening were performed, with studies assessed for risk of bias using the Newcastle-Ottawa scale. A total of 43 studies were identified, studying 1824 patients (724 invasive tumours). Overall, 33 studies identified molecules that were upregulated in invasive tumours, and 20 studies identified molecules that were downregulated. Few studies incorporated modern proteomic or transcriptomic techniques. Risk of bias was low with a mean Newcastle-Ottawa Scale score of 7.0 (± 0.6). Molecules associated with invasion were related to epithelial-mesenchymal transition (E-cadherin, ESRP1, Fascin 1 and MMP-9), cellular proliferation (PTTG,AIP, TCERG1, EIF2β, E2F1,Notch 2, STAT3, ARRB1, TGFB1, SMAD3, SOX9, SGK1, MAGEA6 DLL3, EGFL7 and pEGFR), hormonal signalling (GNAS, DRD5, DRD1, sst5TMD4, SSTR2 and SSTR5) and tumour angiogenesis (VEGF and Drp1). These molecular variations present a possible explanation for the proclivity of somatotropinomas for the cavernous sinus. Identified molecules represent options for novel targeted therapies or biomarkers that could inform prognostication. Modern proteomic and transcriptomic techniques and larger somatotropinoma datasets are required to further elucidate the molecular pathways responsible for cavernous sinus invasion in somatotropinomas. - Source: PubMed
Publication date: 2026/04/16
Ovenden Christopher DillonCandy NicholasBacchi StephenSorvina AlexandraCastle-Kirszbaum MendelPoonnoose SantoshVrodos NikitasJukes AlistairSantoreneos StephenTorpy David JPsaltis AlkisDe Sousa Sunita - TGR5 represents a compelling therapeutic target for metabolic disorders, yet the clinical development of its agonists has been constrained by gallbladder filling. Antagonism of SSTR5 enhances GLP-1 secretion and promotes gallbladder contraction signaling, supporting incretin-mediated glycemic control, and counteracting TGR5-mediated gallbladder filling. Guided by this rationale, a series of dual-target small molecules were rationally designed and synthesized to concurrently activate TGR5 and antagonize SSTR5. Among them, compound (hTGR5 EC = 5.91 nM; hSSTR5 IC = 4.37 nM) exhibited potent and balanced in vitro activity at both TGR5 and SSTR5, although the series displays suboptimal physicochemical and metabolic properties. In vivo, compound improved glucose tolerance and alleviated gallbladder filling at pharmacologically relevant doses. Collectively, these findings establish a proof of concept for dual TGR5/SSTR5 modulation as a promising therapeutic modality, providing a viable strategy to achieve potent metabolic efficacy with reduced risk of adverse effects. - Source: PubMed
Publication date: 2026/04/06
Song ChuhuaWang YuHan XiaoyuLi MengyaGuo ShimengChen LiliSun JunHan FanghuiShi YuqiHu JingZhao JialinWang KaiXie XinShen Jianhua - First-generation somatostatin receptor ligands (SRLs) mainly target SSTR2, whereas neuroendocrine tumors (NETs) often express multiple SSTR subtypes, frequently SSTR5. Dual SSTR2/SSTR5 targeting may enhance anti-hormonal and antiproliferative effects. We evaluated five novel dual SSTR2/SSTR5 agonists (SMTR-001 to SMTR-005) in preclinical NET models to assess their anti-secretory and anti-proliferative effects in representative preclinical NET models. - Source: PubMed
Publication date: 2026/02/27
Fedeli FrancescoBistika MargaritaAscione FrancescoMarangelo AlessandroGuzzi Fabio LSchrader JörgHarris Alan GPellegata Natalia S - Colonic motility is controlled by the enteric nervous system that is modulated not only by autonomic neurotransmitters but also by substances released from enteroendocrine cells. Glucagon-like peptide-1 (GLP-1) secreted from L cells accelerates peristalsis of the proximal colon, whereas somatostatin released from D cells inhibits GLP-1 secretion via the activation of somatostatin receptor subtype 5 (SST). Here, effects of somatostatin on GLP-1-mediated acceleration of colonic peristalsis were investigated. Cannulated segments of rat proximal colon were serosally perfused with oxygenated physiological salt solution and luminally perfused with degassed solution. Colonic wall motion was imaged and converted into spatiotemporal maps. Distributions of somatostatin and SST receptors were assessed via immunohistochemistry. Intraluminal administration of somatostatin alone did not affect oro-aboral propagating peristaltic contractions, but prevented luminal-applied GLP-1 (30 nM)-induced acceleration of peristaltic waves. Somatostatin also prevented the prokinetic action of endogenous GLP-1 that was released upon the stimulation by luminal-applied short-chain fatty acids (SCFA, 3 mM) or lipopolysaccharide. In colonic segments that had been pretreated with selective SST receptor antagonist 1, a lower concentration of GLP-1 (10 nM) or SCFA (300 µM) became capable of accelerating peristaltic waves. GLP-1-positive epithelial cells coexpressed SST receptors, whereas GLP-1 receptor-positive epithelial cells and afferent neurons contained somatostatin. Thus, L cell-derived GLP-1 that accelerates colonic peristalsis may simultaneously stimulate D cells and afferents to release somatostatin that serves as a break on prokinetic actions of GLP-1 by activating SST receptors on L cells. This interplay between GLP-1 and somatostatin would prevent excessive colonic motility. Somatostatin inhibited the prokinetic action of glucagon-like peptide-1 (GLP-1), short-chain fatty acids, and lipopolysaccharide. The inhibitory effect of somatostatin was mediated by the activation of somatostatin receptor subtype 5 that was expressed on L cells. Sources of somatostatin were D cells and intrinsic primary afferent neurons, both of which expressed GLP-1 receptors. Thus, colonic peristalsis may well be regulated by the functional interaction between excitatory GLP-1 and inhibitory somatostatin. - Source: PubMed
Publication date: 2026/01/27
Nakamori HiroyukiHosoi FukoHashitani Hikaru - Polymorphous low-grade neuroepithelial tumors of the young (PLNTY) are slow- or non-progressing epileptogenic tumors, typically occurring in young adults. These tumors are highly calcified and exhibit both diffuse growth and oligodendroglioma-like patterns. Epithelioid glioblastomas (E-GB) are rare and aggressive variants of isocitrate dehydrogenase wildtype glioblastomas (GB), associated with poor overall survival. Both PLNTY and E-GB often carry oncogenic BRAF V600E mutation (BRAF). In this case study, we analyzed clinical and genetic data from a single patient who, based on extensive histological and molecular evaluation, was diagnosed to carry PLNTY-like tumor that progressed into E-GB years later. The aim of our study was to uncover the genetic drivers and the evolutionary history of these tumors. Progression of the PLNTY-like tumor into E-GB was investigated using histology, chromosomal karyotyping, whole-genome sequencing (WGS), and RNA sequencing. A typical immunohistochemical stain pattern of CD34 positivity was detected in the apparent PLNTY, whereas it was depleted in the E-GB sample, as expected. WGS analysis of the PLNTY and three E-GB samples revealed four genes with shared somatic protein-altering mutations: BRAF (carrying BRAF), clonal in both PLNTY and E-GB, as well as GNS, FOXRED2, and SSTR5, which were subclonal in PLNTY and clonal in E-GB. Both the PLNTY-like and E-GB tumors also carried highly similar copy number alteration profiles with a prominent loss of heterozygosity (LOH) in the majority of the chromosomes, suggesting their monoclonal origin. PLNTY-like tumor was mainly diploid, and the tumor underwent a genome-wide duplication event during the progression to E-GB. Furthermore, two focal rearrangements leading to homozygous deletion of CDKN2A/B were detected in E-GB samples. In conclusion, this study revealed unusually extensive LOH in the histologically and genetically supported PLNTY-like tumor that progressed into E-GB. Notably, only a limited set of genetic alterations was associated with malignant transformation beyond genome duplication, the CDKN2A/B inactivation representing the best-known oncogenic driver for malignant transformation. These findings suggest that genomic profiling may be a valuable tool for the diagnosis and prognostic assessment of low-grade neuroepithelial lesions. - Source: PubMed
Publication date: 2026/01/08
Mäntylä SonjaNurminen AnssiHuovinen SannaJaatinen SerafiinaHaapaniemi TeppoNurminen RiikkaHermelo IsmaïlVolz StefanieMaaß Kendra KPajtler Kristian WNordfors KristiinaHaapasalo HannuNykter MattiHaapasalo JoonasRautajoki Kirsi J