ReviewJournal of biomedical science2017
Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions.
Review in Journal of biomedical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Identification of a costimulatory molecule-based signature for predicting prognosis risk and immunotherapy response in patients with lung adenocarcinoma.Oncoimmunology · 2020Pooled it
- The effect and mechanism of TIPE in promoting M2 polarization through DcR3 in the microenvironment of colorectal cancer.Cancer immunology, immunotherapy : CII · 2026Article
- Hirudin Attenuates Uric Acid-Induced Renal Tubular Injury via TNFRSF6B-Mediated Suppression of NF-κB Signaling.Pharmacology research & perspectives · 2026Article
- DcR3 Suppresses Lipopolysaccharide-Induced Aggresome-like Structures in Macrophages via Inhibition of Reactive Oxygen Species and p38 MAPK.International journal of molecular sciences · 2026Article
- Insomnia, proteomic characteristics, and mortality risk in depression: a UK Biobank study.BMC psychiatry · 2026Article
- Decoy Receptors in Autoimmunity: Molecular Guardians and Pathogenic Players in Immune Dysregulation.Mediators of inflammation · 2026Review
- AlphaFold3: A Transformer in Life Sciences.Current medicinal chemistry · 2026Review
- Identification of novel genomic variants in diabetic nephropathy patients using whole-exome sequencing: a pilot investigation.Frontiers in endocrinology · 2026Article
- Bioactive plant and fungal metabolites in oral cancer: molecular mechanisms and translational potential.Frontiers in pharmacology · 2026Review
- The role of tumor necrosis factor receptor superfamily in cancer: insights into oncogenesis, progression, and therapeutic strategies.NPJ precision oncology · 2025Review
- Article
- Defective X-chromosome inactivation and cancer risk in women.Communications biology · 2025Article
- Decoy receptor 3 as a prognostic biomarker for sepsis and septic shock according to the Sepsis-3 definitions.Frontiers in cellular and infection microbiology · 2025Article
- The disruption of NEAT1-miR-125b-5p-SLC1A5 cascade defines the oncogenicity and differential immune profile in head and neck squamous cell carcinoma.Cell death discovery · 2024Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Decoy receptors as biomarkers for exploring aetiology and designing new therapies.Clinical kidney journal · 2024Review
- DcR3-associated risk score: correlating better prognosis and enhanced predictive power in colorectal cancer.Discover oncology · 2024Article
- Article
- Antitumor mechanisms and future clinical applications of the natural product triptolide.Cancer cell international · 2024Review
- Computational design of anti-cancer peptides tailored to target specific tumor markers.BMC chemistry · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decoy receptor 3 (DcR3), also known as tumor necrosis factor receptor (TNFR) superfamily member 6b (TNFRSF6B), is a soluble decoy receptor which can neutralize the biological functions of three members of tumor necrosis factor superfamily (TNFSF): Fas ligand (FasL), LIGHT, and TL1A. In addition to 'decoy' function, recombinant DcR3.Fc is able to modulate the activation and differentiation of dendritic cells (DCs) and macrophages via 'non-decoy' action. DcR3-treated DCs skew T cell differentiation into Th2 phenotype, while DcR3-treated macrophages behave M2 phenotype. DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. However, DcR3-mediated effects in vitro are determined via overexpressing DcR3 or addition of recombinant DcR3.Fc fusion protein. Moreover, CD68-driven DcR3 transgenic mice are used to investigate DcR3-mediated systemic effects in vivo. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion. Thus, 'switch-on' of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while 'switch-off' of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.