Ask about this productRelated genes to: SSTR2 antibody
- Gene:
- SSTR2 NIH gene
- Name:
- somatostatin receptor 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-25
- Date modifiied:
- 2016-10-25
Related products to: SSTR2 antibody
Related articles to: SSTR2 antibody
- Intracranial mesenchymal tumors with FET‑CREB fusion represent a rare tumor entity newly defined in the 5th edition of the WHO classification of central nervous system tumors. Due to overlapping morphological features, these neoplasms were previously diagnosed under different names, including intracranial angiomatoid fibrous histiocytoma and intracranial myxoid mesenchymal tumor. Clinically, they need to be differentiated from meningioma, high‑grade glioma, solitary fibrous tumor, and other intracranial neoplasms. Most supratentorial lesions achieve good outcomes after gross total resection, and tumor recurrence is considered uncommon. We present a 58‑year‑old female patient who experienced local tumor recurrence 27 months after complete resection of a primary supratentorial cystic mass located in the right temporoparieto‑occipital region. The primary lesion was predominantly cystic with minimal solid components. Microscopically, oval and spindle‑shaped tumor cells infiltrated the cystic wall without obvious brain parenchymal invasion, accompanied by linear hemosiderin deposition. Immunohistochemically, tumor cells were diffusely positive for vimentin, MUC4, CD99, synaptophysin, EMA, and ALK (D5F3). Focal positivity was observed for CD68 and broad‑spectrum cytokeratin. All other markers including SMA, MyoD1, HMB45, myogenin, TFE3, MelanA, SOX10, SSTR2, PR, GFAP, and Oligo2 were negative. INI1 expression was intact in all tumor nuclei. The Ki‑67 proliferation index increased from 5%-10% in the primary lesion to 10%-15% in the recurrent specimen. Both primary and recurrent tumors harbored identical EWSR1::ATF1 fusion confirmed by next‑generation sequencing and FISH analysis. The patient received no adjuvant therapy after the first operation, and delayed recurrence was detected during routine MRI follow‑up. A combination of radiological findings, histopathology, immunohistochemistry, and molecular testing is essential for accurate diagnosis of this rare tumor. This case describes late tumor recurrence in an adult patient with typical low‑risk features, including supratentorial location and complete surgical resection. Our findings expand the clinical and pathological spectrum of EWSR1::ATF1‑fused intracranial mesenchymal tumors. Long‑term imaging surveillance is necessary even for patients with favorable clinical factors. Standardized follow‑up protocols and optimal adjuvant treatment strategies remain undefined and require further validation in larger cohorts. - Source: PubMed
Publication date: 2026/09/29
Xiu YueLi QihangZhou QuanWang Xiangyue - G protein-coupled receptors (GPCRs) are the target for approximately 36% of approved drugs and control many cell signaling pathways. Among these is the somatostatin receptor 2 (SSTR2), which can be targeted by the radiolabeled somatostatin analog [Lu]Lu-DOTA-Tyr-octreotate (Lu-DOTATATE) for treatment of neuroendocrine cancers. Here, we provide a detailed kinetic characterization of the uptake and retention dynamics for Lu-DOTATATE binding to SSTR2 on live tumor cells to gain a deeper understanding on how observed binding affinities relate to receptor biology and subsequent treatment outcome. Real-time cell binding assays have revealed two main interaction populations distinguished primarily by their retention times. High-affinity binding in the sub-nanomolar range was associated with Lu-DOTATATE interacting with G protein-coupled receptors, whereas low-affinity binding in the nanomolar range corresponded to interactions with uncoupled receptors. Cells fixed prior to ligand exposure also exhibited high-affinity binding, although to a lesser degree, implying the presence of pre-coupled SSTR2. Cellular retention decreased with ligand exposure, suggesting a shift in receptor coupling state after prolonged stimulation. Intracellular accumulation upon ligand stimulation was confirmed for both Lu-DOTATATE and SSTR2. Unlabeled DOTATATE was able to induce excretion of internalized Lu-DOTATATE, revealing a highly dynamic interaction with constant turnover of ligands. This study highlights the dynamic nature of agonists binding to GPCRs in a live cell environment. By employing cell-based real-time binding assays, we were able de-convolute the contribution of distinct receptor states to Lu-DOTATATE affinity and retention and study the impact of internalization and recycling dynamics. Improved understanding of ligand/drug-GPCR interactions and how these are impacted by the cellular environment and metabolism can be used to optimize existing and new therapeutic approaches. - Source: PubMed
Salomonsson Sara LundstenEngbers Pleun A MNonnekens JulieBondza Sina - : Herein, we report on the development of a novel submicron-sized formulation that utilizes the somatostatin receptor agonist, octreotide (OCT), for the solubilization and targeted delivery of paclitaxel (PTX) and docetaxel (DTX) to the cancer cells. The formulation was prepared using a fast, single-step, and scalable method, and then, it was characterized in terms of physicochemical properties and pharmacological activities. : Formulation analyses by Electrospray Ionization Mass Spectrometry (ESI-MS) and High-Performance Liquid Chromatography (HPLC) confirmed the successful formation of the formulation and the inclusion of all of its components. Meanwhile, the developed formulation showed acceptable physicochemical properties with no incompatibilities among its components. In addition, the prepared formulation, OCT-PTX-DTX, demonstrated superior anticancer activities against colorectal carcinoma cell lines compared to the free drugs, with minimal effects on the normal cells. Furthermore, a synergistic anticancer activity of PTX and DTX was enabled by the novel formulation, leading to cell cycle arrest at low drug concentrations. : Molecular-based mechanistic investigations verified that OCT-PTX-DTX is taken up by colorectal cancer cells via somatostatin receptors 1 and 2 (SSTR1 and SSTR2), followed by the upregulation of the tumor-suppressor p53/p21 cascade, and the induced cell cycle arrest via suppression of the cell cycle drivers CDK2 and Cyclin A. The formulation reported herein is promising for targeted and biotolerable anticancer chemotherapy compared to the commercially available taxane formulations based on surfactants or organic solvents. - Source: PubMed
Publication date: 2026/09/15
Abdellatif Ahmed A HTawfeek Hesham MEl-Readi Mahmoud ZakiAlharbi Amani EMaswadeh Hamzah MAmin Mohammed AEid Safaa YEllethy Abousree TRefaat BassemAslam AkhmedAltowayan Waleed MohammadYounis Mahmoud A - Clinically non-functioning pituitary neuroendocrine tumors (NF-PitNETs) lack effective medical therapies, and the role of somatostatin receptor ligands (SRLs) and dopamine agonists (DAs) in this setting is controversial. We evaluated the in vitro response of NF-PitNETs to multiple SRL and/or DA treatments, focusing on the role of receptor expression and tumor characteristics in driving tumor response. Forty-four NF-PitNET primary cultures were treated (72 h, 10 nM) with octreotide (OCT), pasireotide (PAS), OCT + PAS, BIM-53097 (D2R agonist), BIM-53097 + PAS, and BIM-23B065 (SSTR2/SSTR5/D2R preferential ligand) to evaluate cell proliferation inhibition. Tumors were considered responders to a treatment when a ≥20% reduction in cell proliferation was observed (vs. control); responder tumors to at least one tested condition were classified into the "responder group" for further analysis. Somatostatin (SSTRs) and dopamine type 2 receptor (D2R) expression were evaluated through immunohistochemistry. Data on radiological invasiveness, proliferation indices (Ki67%, mitoses), and p53 immunostaining were collected. Tumor grade was determined using Trouillas and PANOMEN-3 classifications. Median patient age at surgery was 60.3 years (IQR 49.7-70.7), 29 were males (71%). Overall, no significant in vitro inhibition of cell proliferation was observed [ranging from -4.2% (OCT and PAS) to -7.4% (BIM-53097 + PAS)]. However, 13 cultures (30%) were included in the "responder group" [mean inhibition ranging from -18.6% (OCT) to -27.7% (BIM-53097 + PAS)]. D2R was the most expressed receptor (median IRS 8, IQR 6-8), followed by SSTR1 and SSTR2 (median IRS 4, IQR 3-6); SSTR3 and SSTR5 expression was low. In the whole cohort, OCT and PAS efficacy directly correlated with SSTR2 (p = .013 and p = .027, respectively). D2R and SSTR2 expression was higher in responders vs. non-responders to BIM-23B065 (p = .017 and p = .042, respectively). ROC curve analysis discriminates BIM-23B065 responders based on D2R and SSTR2 expression with acceptable ability (AUC = 0.784 and AUC = 0.743, respectively). However, the "responder group" did not differ significantly from the "non-responder group" with respect to patient demographics, tumor clinical-pathological characteristics, receptor expression, and grading. In conclusion, we confirm the limited efficacy of SRL and DA treatment in NF-PitNETs. D2R and SSTR2 can discriminate tumors responsive to BIM-23B065. As concerns the other tested compounds, none of the tumor parameters evaluated demonstrated robust predictive value for NF-PitNET in vitro response. - Source: PubMed
Campana ClaudiaAmarù JessicaRossi Diego CriminelliArecco AnnaNozza PaoloBoschetti MaraZona GianluigiFerone DiegoArvigo MaricaGatto Federico - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and pathological hallmarks such as amyloid-beta (Aβ) deposition and tau hyperphosphorylation. Increasing evidence identifies mitochondrial dysfunction as an early and central driver of AD pathogenesis, contributing to impaired bioenergetics, oxidative stress, disrupted calcium homeostasis, and synaptic failure. Notably, somatostatin (SST), a neuropeptide significantly reduced in AD brains, has emerged as a candidate regulator of neuronal metabolism and mitochondrial homeostasis. In this review, we propose a conceptual and testable framework linking reduced SST signaling to mitochondrial dysfunction in AD. Current evidence most directly supports effects of SST signaling on neuronal excitability and calcium homeostasis, whereas direct evidence linking SST or individual SSTR subtypes-particularly SSTR2 and SSTR4-to mitochondrial bioenergetics, mitophagy, cristae organization, and mitochondrial dynamics remains limited and is discussed here largely at the level of plausible, testable hypotheses. Downstream signaling pathways, including Gi-coupled inhibition of cAMP/PKA and modulation of PI3K/Akt, have established roles in neuronal signaling and are discussed here in relation to their potential, but not yet directly demonstrated, contributions to mitochondrial bioenergetics, redox balance, calcium handling, mitophagy, and mitochondrial dynamics. Disruption of these processes may plausibly contribute to a self-amplifying cycle involving Aβ accumulation, tau pathology, and synaptic dysfunction, although this cycle has not been directly demonstrated for SST signaling specifically. Collectively, the SST-mitochondria axis represents a conceptual and testable framework that may help explain aspects of AD pathogenesis, pending direct mechanistic validation, offering promising therapeutic opportunities beyond conventional amyloid- and tau-centric approaches. Future research should focus on receptor subtype-specific mechanisms, mitophagy modulation, and mitochondrial calcium regulation to advance translational applications. - Source: PubMed
Publication date: 2026/09/24
Liu KaiZhang Xi-YuQiu Hong-BoSu Chen-QiWang Shao-YunPei Zi-JunJin Run-HaoBing Yan-Hua