ArticleFrontiers in pharmacology2024
Urolithin A increases the natural killer activity of PBMCs in patients with prostate cancer.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Urolithin A alleviates vascular remodeling through mitochondrial SIRT3-mediated SOD2 deacetylation and antioxidation in hypertensive rats.Redox report : communications in free radical research · 2026Article
- Review
- Urolithin A blocks colorectal cancer progression by AKT1 inhibition-driven immune activation.Scientific reports · 2026Article
- Unraveling the microbial landscape in prostate cancer: pathogenesis to therapy.NPJ biofilms and microbiomes · 2026Review
- Gut microbial metabolites in cancer immunomodulation.Molecular cancer · 2025Review
- NK Cell-Microbiota Interaction Biomarker Strategy: Advancing Prostate Cancer Management.Biomolecules · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: The natural killer (NK) activity of peripheral blood mononuclear cells (PBMCs) is a crucial defense against the onset and spread of cancer. Studies have shown that patients with reduced NK activity are more susceptible to cancer, and NK activity tends to decrease due to cancer-induced immune suppression. Enhancing the natural cytotoxicity of PBMCs remains a significant task in cancer research. Methods: This study investigates the potential of urolithin A, a polyphenolic metabolite produced by the gut microbiota, to enhance the natural cytotoxicity of PBMCs in prostate cancer patients and healthy subjects. We investigated the possible role of aryl hydrocarbon receptor (AhR) in this capability of urolithin A. We analyzed the ability of PBMCs preincubated with urolithin A, AhR agonist or antagonist to kill K562 (human chronic myelogenous leukemia) target cells. Results: Our results demonstrate that urolithin A enhances the natural cytotoxicity of PBMCs in a dose-dependent manner. Specifically, at a concentration of 10 μM, urolithin A increased the NK activity of PBMCs from prostate cancer patients by an average of 23% (95% CI, 7%-38%). In addition, urolithin A modulates the level of cytokine production by PBMCs, decreasing the level of fractalkine, IL-8, and MCP-3. An AhR antagonist (CH223191, 1 μM) also increased NK activity, while an AhR agonist (β-naphthoflavone, 10 μM) did not increase NK activity and partially inhibited the urolithin A-induced enhancement. Conclusion: Urolithin A increases the NK activity of PBMCs from patients with prostate cancer and healthy subjects, and the AhR may be involved in this capability of urolithin A.
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