ArticlePloS one2018
Tumor-secreted factors induce IL-1β maturation via the glucose-mediated synergistic axis of mTOR and NF-κB pathways in mouse macrophages.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- MAPK Inhibitor-Tolerant Persister Cells in Melanoma: Mechanisms and Therapeutic Vulnerabilities.Cancer science · 2026Review
- Macrophage Immunometabolism in Epicardial Adipose Tissue and Obesity-Related Atrial Fibrillation.Journal of inflammation research · 2026Review
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
- The photosensitizer DH-I-180-3 regulates intracellular bacterial growth by increasing the secretion of proinflammatory cytokines via the NF-κB- and MAPK-mediated signaling pathways and promoting phagosome maturation in Salmonella-infected mouse macrophages.Journal of microbiology (Seoul, Korea) · 2025Article
- Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.Cancer communications (London, England) · 2024Review
- Thymoquinone, a Novel Multi-Strike Inhibitor of Pro-Tumorigenic Breast Cancer (BC) Markers: CALR, NLRP3 Pathway and sPD-L1 in PBMCs of HR+ and TNBC Patients.International journal of molecular sciences · 2023Article
- Identification of Immune-Related lncRNA Pairs and Construction and Validation of a New Prognostic Signature of Colon Cancer.Canadian journal of gastroenterology & hepatology · 2022Article
- The Signaling Pathways Regulating NLRP3 Inflammasome Activation.Inflammation · 2021Review
- Rapamycin Promotes ROS-Mediated Cell DeathFrontiers in oncology · 2021Article
- Lysophosphatidylcholine Enhances Bactericidal Activity by Promoting Phagosome Maturation via the Activation of the NF-κB Pathway duringMolecules and cells · 2020Article
- Metabolism in tumour-associated macrophages: aEuropean respiratory review : an official journal of the European Respiratory Society · 2020Review
- Influence of the Hippo-YAP signalling pathway on tumor associated macrophages (TAMs) and its implications on cancer immunosuppressive microenvironment.Annals of translational medicine · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are one of the major cell types that produce IL-1β. IL-1β maturation occurs via inflammasome activation, and mature IL-1β is then released from the cell. Secreted IL-1β mediates inflammatory reactions in various pathological environments, such as those in infectious, autoimmune, and cancerous diseases. Although the mechanism of IL-1β production has been discovered in infectious and autoimmune diseases, its production mechanism in the tumor microenvironment is unclear. Therefore, the mechanism of IL-1β production in macrophages in the tumor microenvironment was investigated in this study. First, bone marrow-derived macrophages obtained from C57BL/6 mice were treated with B16F10 tumor-conditioned media (TCM) in vitro. TCM increased the levels of IL-1β via glucose-mediated activation of the inflammasome. Moreover, TCM enhanced the activation of both NF-κB and mTOR pathways in a glucose-dependent manner. In particular, the expression levels of mTORC1 component proteins were dependent on the TCM-induced activation of NF-κB signaling. In addition, TCM affected ASC-ASC interactions through increasing intracellular reactive oxygen species levels. Finally, glucose inhibition by inoculation with 2-deoxy-D-glucose in vivo decreased the IL-1β levels in both the blood and tumor region of B16F10-bearing C57BL/6 mice relative to those in PBS-injected tumor-bearing mice. These results suggest that glucose supplied from blood vessels might be important for IL-1β production in tumor-associated macrophages via the integrated signals of the NF-κB and mTOR pathways in the tumor microenvironment.
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