ArticleThe Journal of clinical investigation2016
NLRC4 suppresses melanoma tumor progression independently of inflammasome activation.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026Pooled it
- Current understanding of the NLRC4 Inflammasome in autoinflammation and enterocolitis.Communications biology · 2026Review
- Plasma NLRC4 and NLRP3 as potential diagnostic biomarkers for non-small cell lung cancer in pulmonary tuberculosis.Discover oncology · 2025Article
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- Inflammasome activation in melanoma progression: the latest update concerning pathological role and therapeutic value.Archives of dermatological research · 2025Review
- The mycobiome in human cancer: analytical challenges, molecular mechanisms, and therapeutic implications.Molecular cancer · 2025Review
- Regulation of cancer by inflammasomes: from inflammation to tumorigenesis.Frontiers in immunology · 2025Review
- Neuroinflammatory Proteins in Huntington's Disease: Insights into Mechanisms, Diagnosis, and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Inflammasome protein scaffolds the DNA damage complex during tumor development.Nature immunology · 2024Article
- NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024Review
- New prospects of cancer therapy based on pyroptosis and pyroptosis inducers.Apoptosis : an international journal on programmed cell death · 2024Review
- LNCGM1082 in Gut Epithelial Cells Promotes Expulsion of Infected Epithelial Cells and Release of IL-18.ImmunoHorizons · 2024Article
- Development and validation of an immune-related gene prognostic index for lung adenocarcinoma.Journal of thoracic disease · 2023Article
- Identifying prognostic genes related PANoptosis in lung adenocarcinoma and developing prediction model based on bioinformatics analysis.Scientific reports · 2023Article
- Pyroptosis and inflammasomes in cancer and inflammation.MedComm · 2023Review
- Inflammasomes as regulators of non-infectious disease.Seminars in immunology · 2023Review
- Canonical Inflammasomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The roles of inflammasomes in cancer.Frontiers in immunology · 2023Review
- A novel pyroptosis-related prognostic signature for lung adenocarcinoma: Identification and multi-angle verification.Frontiers in genetics · 2023Article
- Mechanism of inflammasomes in cancer and targeted therapies.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Members of the NLR family can assemble inflammasome complexes with the adaptor protein ASC and caspase-1 that result in the activation of caspase-1 and the release of IL-1β and IL-18. Although the NLRC4 inflammasome is known to have a protective role in tumorigenesis, there is an increased appreciation for the inflammasome-independent actions of NLRC4. Here, we utilized a syngeneic subcutaneous murine model of B16F10 melanoma to explore the role of NLRC4 in tumor suppression. We found that NLRC4-deficient mice exhibited enhanced tumor growth that was independent of the inflammasome components ASC and caspase-1. Nlrc4 expression was critical for cytokine and chemokine production in tumor-associated macrophages and was necessary for the generation of protective IFN-γ-producing CD4+ and CD8+ T cells. Tumor progression was diminished when WT or caspase-1-deficient, but not NLRC4-deficient, macrophages were coinjected with B16F10 tumor cells in NLRC4-deficient mice. Finally, examination of human primary melanomas revealed the extensive presence of NLRC4+ tumor-associated macrophages. In contrast, there was a paucity of NLRC4+ tumor-associated macrophages observed in human metastatic melanoma, supporting the concept that NLRC4 expression controls tumor growth. These results reveal a critical role for NLRC4 in suppressing tumor growth in an inflammasome-independent manner.
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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.