ArticleScientific reports2017
Canonical NFκB signaling in myeloid cells is required for the glioblastoma growth.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Challenges in Developing a Microglial NF-Kappa B Conditional Mouse Model for Glioblastoma Studies.Cells · 2026Article
- Expression of NF-κB Isoforms and IKK Complex Subunits Differs in Peripheral Blood Mononuclear Cells (PBMCs) of Patients with Meningiomas: A Pilot Study.Life (Basel, Switzerland) · 2026Article
- Orchestration of Tumor-Associated Macrophages in the Tumor Cell-Macrophage-CD8International journal of biological sciences · 2025Review
- Microfluidic-Derived Docosahexaenoic Acid Liposomes for Targeting Glioblastoma and Its Inflammatory Microenvironment.ACS applied materials & interfaces · 2024Article
- Intratumoral delivery of the chitin-derived C100 adjuvant promotes robust STING, IFNAR, and CD8Cell reports. Medicine · 2024Article
- Understanding the immunosuppressive microenvironment of glioma: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
- NF-κB: Governing Macrophages in Cancer.Genes · 2024Review
- Peritumoral brain zone in glioblastoma: biological, clinical and mechanical features.Frontiers in immunology · 2024Review
- Production of a p65Innate immunity · 2023Article
- Targeting Options of Tumor-Associated Macrophages (TAM) Activity in Gliomas.Current neuropharmacology · 2023Review
- Regional infusion of a class C TLR9 agonist enhances liver tumor microenvironment reprogramming and MDSC reduction to improve responsiveness to systemic checkpoint inhibition.Cancer gene therapy · 2022Article
- Phosphoinositide 3-kinase/Akt and its related signaling pathways in the regulation of tumor-associated macrophages polarization.Molecular and cellular biochemistry · 2022Review
- The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity.International journal of molecular sciences · 2022Review
- Chemerin enhances mesenchymal features of glioblastoma by establishing autocrine and paracrine networks in a CMKLR1-dependent manner.Oncogene · 2022Article
- Article
- The Hallmarks of Glioblastoma: Heterogeneity, Intercellular Crosstalk and Molecular Signature of Invasiveness and Progression.Biomedicines · 2022Review
- Necrotic reshaping of the glioma microenvironment drives disease progression.Acta neuropathologica · 2022Review
- Gas Plasma Exposure of Glioblastoma Is Cytotoxic and Immunomodulatory in Patient-Derived GBM Tissue.Cancers · 2022Article
- Tumor-associated microglia and macrophages in glioblastoma: From basic insights to therapeutic opportunities.Frontiers in immunology · 2022Review
- Tumor-Associated Microglia and Macrophages in the Glioblastoma Microenvironment and Their Implications for Therapy.Cancers · 2021Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor development and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived suppressor cell (MDSC) infiltration in tumors via chemokine axis. Chemokine expression, which determines the pro or anti-inflammatory status of myeloid cells, are partly regulated by the nuclear factor-kappa B (NF-κB) pathway. Here, we identified that conditional deletion of canonical NF-κB signaling (p65) in myeloid cells inhibited syngeneic glioblastoma (GBM) through decreased CD45 infiltration in tumors, as characterized by decreased TAMs (CD206+) and MDSCs (Gr1+ CD11b+), increased dendritic cells (CD86+) and cytotoxic T cells (CD8+) in the p65 knockout (KO) mice. Proinflammatory cytokines (IFNγ, MCP1, MIP1α, and TNFα) and myeloid differentiation factor (Endoglin) were increased in myeloid cells from p65 KO tumor, which demonstrated an influence on CD8+T cell proliferation. In contrast, p65KO athymic chimeric mice with human GBM, failed to inhibit tumor growth, confirming the contribution of T cells in an immune competent model. The analysis of human datasets and GBM tumors revealed higher expression of p65 in GBM-associated CD68+ macrophages compared to neighboring stroma. Thus, canonical NF-κB signaling has an anti-inflammatory role and is required for macrophage polarization, immune suppression, and GBM growth. Combining an NF-κB inhibitor with standard therapy could improve antitumor immunity in GBM.
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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.