ArticleFrontiers in immunology2023
Macrophage IL-1β contributes to tumorigenesis through paracrine AIM2 inflammasome activation in the tumor microenvironment.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- PANoptosis and Immune Remodeling in the Tumor Microenvironment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Myeloid miR-155 deficiency exacerbates viral encephalitis by hindering M1 macrophage polarization due to impaired NLRP3 inflammasome activation in extraneural tissues.Frontiers in immunology · 2026Article
- Semaphorin-7A promotes macrophage-mediated mammary epithelial and ductal carcinoma in situ invasion.Breast cancer research : BCR · 2025Article
- Synergistic overcoming of cisplatin resistance in ovarian cancer by combined Astragalus Membranaceus and cisplatin treatment: network pharmacology and experimental validation.BMC complementary medicine and therapies · 2025Article
- The immune-related prognostic gene AIM2 promotes pancreatic cancer progression via inflammasome.Scientific reports · 2025Article
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- rFIP-nha activates macrophages towards a pro-inflammatory phenotype via AIM2 inflammasome modulation.Frontiers in cell and developmental biology · 2025Article
- The Role of AIM2 in Cancer Development: Inflammasomes and Beyond.Journal of Cancer · 2025Review
- Engineering cGAS-agonistic oligonucleotides as therapeutics for cancer immunotherapy.Molecular therapy. Nucleic acids · 2024Article
- Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review.Cancers · 2023Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular recognition of self and non-self -nucleic acids can result in the initiation of effective pro-inflammatory and anti-tumorigenic responses. We hypothesized that macrophages can be activated by tumor-derived nucleic acids to induce inflammasome activation in the tumor microenvironment. We show that tumor conditioned media (CM) can induce IL-1β production, indicative of inflammasome activation in primed macrophages. This could be partially dependent on caspase 1/11, AIM2 and NLRP3. IL-1β enhances tumor cell proliferation, migration and invasion while coculture of tumor cells with macrophages enhances the proliferation of tumor cells, which is AIM2 and caspase 1/11 dependent. Furthermore, we have identified that DNA-RNA hybrids could be the nucleic acid form which activates AIM2 inflammasome at a higher sensitivity as compared to dsDNA. Taken together, the tumor-secretome stimulates an innate immune pathway in macrophages which promotes paracrine cancer growth and may be a key tumorigenic pathway in cancer. Broader understanding on the mechanisms of nucleic acid recognition and interaction with innate immune signaling pathway will help us to better appreciate its potential application in diagnostic and therapeutic benefit in cancer.
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