SSTR3 as a Radioligand Therapy Target
SSTR3, somatostatin receptor 3, is a cell-surface protein (GPCR). In Human Protein Atlas immunohistochemistry, SSTR3 staining is highest in bladder cancer (58% of samples positive), colorectal cancer (50% of samples positive) and neuroendocrine tumors (50% of samples positive). Published literature reports that SSTR3 internalizes after ligand binding, which helps retain a radionuclide inside tumor cells. Clinical status: Clinical-stage (up to phase 3, any modality).
Is SSTR3 a good radioligand therapy target?
Scored against the six criteria that decide whether a protein can become a radioligand therapy:
- ✅ Cell-surface accessibility: Localized to the cell surface, so a radioligand can reach it from circulation.
- ⚠️ Tumor expression: Medium IHC staining in bladder cancer, 58% of samples positive.
- ✅ Internalization: Reported to internalize, which favors radionuclide retention.
- ✅ Clinical precedent: Clinical-stage (up to phase 3, any modality)
- ❔ Shedding: Not yet assessed.
- ❔ Normal-tissue dosimetry: Check kidney, liver, bone marrow and salivary expression in the Human Protein Atlas tissue atlas.
SSTR3 expression in cancer
Protein expression of SSTR3 across 20 cancer types from Human Protein Atlas immunohistochemistry. The score is a weighted staining intensity from 0 to 1; "% positive" is the share of patient samples with detectable staining.
| Cancer type | IHC score | Level | % positive |
|---|---|---|---|
| Bladder Cancer | 0.28 | Medium | 58% |
| Colorectal Cancer | 0.25 | Medium | 50% |
| Neuroendocrine Tumors | 0.25 | Medium | 50% |
| Cervical Cancer | 0.21 | Medium | 46% |
| Endometrial Cancer | 0.15 | Low | 44% |
| Breast Cancer | 0.12 | Low | 27% |
| Ovarian Cancer | 0.11 | Low | 22% |
| Pancreatic Cancer | 0.07 | Low | 20% |
| Glioma | 0.07 | Low | 10% |
| Gastric Cancer | 0.06 | Low | 17% |
| Liver Cancer | 0.06 | Low | 17% |
| Kidney Cancer | 0.03 | Low | 8% |
Not detected by IHC in: skin cancer, head and neck cancer, lymphoma, melanoma, thyroid cancer, lung cancer, prostate cancer, testicular cancer.
Is SSTR3 internalized?
Yes. ITF2984 induces receptor internalization and phosphorylation, and triggers G-protein signaling at pharmacologically relevant concentrations.
Sources: PMID 37444563 · PMID 36857170 · PMID 27375434 · PMID 24587133 · PMID 23116418. AI-extracted from abstracts, so verify before citing.
SSTR3 clinical trials
Clinical-stage (up to phase 3, any modality). Nuclens hasn't indexed trials for SSTR3 yet. Search ClinicalTrials.gov for SSTR3 trials.
SSTR3 normal tissue expression
Normal-tissue expression in dose-limiting organs (kidney, liver, bone marrow, salivary glands) drives radioligand dosimetry risk. Nuclens is re-validating its normal-tissue values, so they are not shown here yet. See SSTR3 in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
SSTR3 gene essentiality (DepMap)
CRISPR knockout effect across 1241 cancer cell lines: -0.02 (not essential). Radioligands kill by radiation, not by blocking the target, so essentiality matters less than for inhibitors. A non-essential target can still be an excellent radioligand target.
Related bladder cancer radioligand targets
EGFR · HER3 (ERBB3) · c-MET (MET) · SSTR2 · ITGAV · HER2 (ERBB2) · B7-H3 (CD276) · FAP
See all radioligand therapy targets in bladder cancer.
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Subcellular localization: UniProt via Open Targets (CC BY 4.0 / CC0). Tumor immunohistochemistry: Human Protein Atlas (CC BY-SA 4.0). Clinical trials: ClinicalTrials.gov (public domain). Gene essentiality: DepMap (CC BY 4.0). Internalization and shedding: AI-extracted from PubMed abstracts, so verify against the cited papers before relying on them. Nuclens is a first-pass triage layer, not a substitute for wet-lab validation or clinical dosimetry. Derived expression data on this page is shared under CC BY-SA 4.0.