ArticleFrontiers in oncology2020
Inflammasome Deletion Promotes Anti-tumor NK Cell Function in an IL-1/IL-18 Independent Way in Murine Invasive Breast Cancer.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Molecular Mechanism of NLRP3 Inflammasome in Inflammatory Diseases and Tumors.Immunity, inflammation and disease · 2025Review
- Molecular insights into NLRP3 inflammasome and miRNA modulation in oral cancer.Frontiers in pharmacology · 2025Review
- Inhibition of NLRP3 inflammasome contributes to paclitaxel efficacy in triple negative breast cancer treatment.Scientific reports · 2024Article
- Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024Review
- Divergent functions of NLRP3 inflammasomes in cancer: a review.Cell communication and signaling : CCS · 2023Review
- Downstream Signaling of Inflammasome Pathway Affects Patients' Outcome in the Context of Distinct Molecular Breast Cancer Subtypes.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Pan-cancer analysis of prognostic and immunological role of DTYMK in human tumors.Frontiers in genetics · 2022Article
- Inflammasomes in Cancer Progression and Anti-Tumor Immunity.Frontiers in cell and developmental biology · 2022Review
- NLRP3 inflammasome-mediated cytokine production and pyroptosis cell death in breast cancer.Journal of biomedical science · 2021Review
- Prognostic Value of NLRP3 Inflammasome and TLR4 Expression in Breast Cancer Patients.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Inflammasomes are molecular complexes that trigger an inflammatory response upon detection of pathogens or danger signals. Recent studies suggest that they are also involved in cancer progression. However, their roles during tumorigenesis remain poorly understood and controversial. Here, we investigated whether inflammasome activation supports mammary tumor growth. Using mouse models of invasive breast cancer, our results demonstrate that the absence of a functional inflammasome impairs tumor growth. Importantly, tumors implanted into inflammasome-deficient mice recruited significantly less neutrophils and more natural killer (NK) cells, and these latter cells displayed a more active phenotype. Interestingly, NK cell depletion abolished the anti-tumoral effect observed in inflammasome-deficient mice, although inflammasome-regulated cytokine neutralization had no effect. Thus, our work identifies a novel role for the inflammasome in supporting mammary tumor growth by attenuating NK cell recruitment and activity. These results suggest that inflammasome inhibition could be a putative target for treating invasive breast cancers.
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