ArticleNature communications2020
Targeting FROUNT with disulfiram suppresses macrophage accumulation and its tumor-promoting properties.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 105 citations in OpenAlex.
- Disulfiram ameliorates nonalcoholic steatohepatitis by modulating the gut microbiota and bile acid metabolism.Nature communications · 2022Trial
- Disulfiram Alleviates Metabolic Dysfunction-Associated Steatohepatitis in Mice via Inhibiting Aurora Kinase A and Restoring Autophagy.Antioxidants (Basel, Switzerland) · 2026Article
- Therapeutic repurposing of old drugs to modulate the tumor immune microenvironment and enhance immunotherapy efficacy.Journal of pharmaceutical analysis · 2026Review
- Aldehyde dehydrogenase 1 A1 regulates the transcription of PD-L1 and its targeting with disulfiram together with PD-L1 immunotherapy synergistically delays cyst growth in ADPKD.Kidney international · 2026Article
- Cuproptosis-based nanomedicine in cancer metastasis synergistic therapy.Acta pharmaceutica Sinica. B · 2026Review
- Exploring the therapeutic potential of disulfiram in endometriosis: mechanisms targeting inflammation, oxidative stress, pyroptosis, and angiogenesis.Archives of gynecology and obstetrics · 2026Review
- NPLOC4 Inhibition Remodels Tumor Microenvironment via M2-to-M1 Macrophage Reprogramming and Boosts Anti-PD-1 Response in Liver Cancer.International journal of biological sciences · 2026Article
- NUP85 as a Pan-Cancer Immune Biomarker: Integrated Multi Omics and Functional Analyses Reveal Its Role in Tumor Prognosis.ImmunoTargets and therapy · 2026Article
- NUP85 siRNA loaded red blood cell-derived extracellular vesicles alleviate hepatic steatosis in MASLD.Journal of nanobiotechnology · 2025Article
- Disulfiram as an anti-inflammatory agent: mechanisms, nano-delivery strategies, and applications in non-oncologic diseases.RSC advances · 2025Review
- Immune checkpoint molecules signal regulatory protein alpha in the development of hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Review
- A CD4+ T lymphocyte-specific TCR/GSDMD/IL-2 axis facilitates antitumor immunity.The Journal of clinical investigation · 2025Article
- The Current State of Tumor Microenvironment-Specific Therapies for Non-Small Cell Lung Cancer.Cancers · 2025Review
- Vitamin A Metabolism and Resistance of Hepatic Metastases to Immunotherapy.Molecular cancer therapeutics · 2025Review
- Disulfiram ameliorates bone loss in ovariectomized mice by suppressing osteoclastogenesis.Journal of bone and mineral metabolism · 2025Article
- Repurposing alcohol-abuse drug disulfiram for the treatment of KSHV-infected primary effusion lymphoma by activating antiviral innate immunity.PLoS pathogens · 2025Article
- Disulfiram potentiates cisplatin-induced apoptosis in small cell lung cancer via the inhibition of cystathionine β-synthase and HAmerican journal of cancer research · 2025Article
- Disulfiram/copper triggers cGAS-STING innate immunity pathway via ROS-induced DNA damage that potentiates antitumor response to PD-1 checkpoint blockade.International journal of biological sciences · 2025Article
- Sirp-α Antibody Inhibits Renal Cell Carcinoma Progression via Akt1/Akt2 Modulation in Tumor-Associated Macrophages.Journal of inflammation research · 2025Article
- Drug functional remapping: a new promise for tumor immunotherapy.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
27 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages affect tumor progression and resistance to immune checkpoint therapy. Here, we identify the chemokine signal regulator FROUNT as a target to control tumor-associated macrophages. The low level FROUNT expression in patients with cancer correlates with better clinical outcomes. Frount-deficiency markedly reduces tumor progression and decreases macrophage tumor-promoting activity. FROUNT is highly expressed in macrophages, and its myeloid-specific deletion impairs tumor growth. Further, the anti-alcoholism drug disulfiram (DSF) acts as a potent inhibitor of FROUNT. DSF interferes with FROUNT-chemokine receptor interactions via direct binding to a specific site of the chemokine receptor-binding domain of FROUNT, leading to inhibition of macrophage responses. DSF monotherapy reduces tumor progression and decreases macrophage tumor-promoting activity, as seen in the case of Frount-deficiency. Moreover, co-treatment with DSF and an immune checkpoint antibody synergistically inhibits tumor growth. Thus, inhibition of FROUNT by DSF represents a promising strategy for macrophage-targeted cancer therapy.
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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.