ArticleOncology research2019
NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals.
Article in Oncology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Transcriptomic Evidence Identifies Two TMBIM Subgroups with Opposing Prognostic Associations in Glioma.Biology · 2026Article
- Review
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
- Innate Immune Signaling in Gliomas: Regulatory Mechanisms and Targeting Potential in Tumor Progression.Life (Basel, Switzerland) · 2025Review
- The Role of Sirt1 in Regulating Inflammatory Cytokines and Oxidative Stress in the Transition Mechanism from Depressive Disorder to Alzheimer's Disease.Molecular neurobiology · 2025Article
- NLRP3 Inflammasome Activation Expands the Immunosuppressive Myeloid Stroma and Antagonizes the Therapeutic Benefit of STING Activation in Glioblastoma.Cancer research communications · 2025Article
- Mechanistic insights curcumin's anti-inflammatory in pancreatic cancer: experimental and computational evidence implicating IL1B interferenceFrontiers in cell and developmental biology · 2025Article
- The role of NLRP3 and NLRP12 inflammasomes in glioblastoma.Genes and immunity · 2024Review
- Caspase-4 in glioma indicates deterioration and unfavorable prognosis by affecting tumor cell proliferation and immune cell recruitment.Scientific reports · 2024Article
- Role of NLRP3 inflammasome in central nervous system diseases.Cell & bioscience · 2024Review
- Sphingolipid Signaling and Complement Activation in Glioblastoma: A Promising Avenue for Therapeutic Intervention.BioChem · 2024Article
- Resveratrol ameliorates glioblastoma inflammatory response by reducing NLRP3 inflammasome activation through inhibition of the JAK2/STAT3 pathway.Journal of cancer research and clinical oncology · 2024Article
- Comparative assessment of direct and indirect cold atmospheric plasma effects, based on helium and argon, on human glioblastoma: an in vitro and in vivo study.Scientific reports · 2024Article
- Deciphering sources of PET signals in the tumor microenvironment of glioblastoma at cellular resolution.Science advances · 2023Article
- The 'speck'-tacular oversight of the NLRP3-pyroptosis pathway on gastrointestinal inflammatory diseases and tumorigenesis.Journal of biomedical science · 2023Review
- Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023Review
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- Article
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- Relevance of the pyroptosis-related inflammasome drug targets in the Chuanxiong to improve diabetic nephropathy.Molecular medicine (Cambridge, Mass.) · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1β, IL-1β antibody, and NF-κB inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected by PCR, Western blot, and ELISA. NLRP3 and NF-κB p65 increased and were positively correlated in glioma tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1β and NF-κB p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous IL-1β-elevated cell proliferation and invasion, whereas IL-1β elimination impaired the proproliferation effect of NLRP3 hyperexpression. Furthermore, NF-κB blockage abrogated IL-1β and NLRP3 hyperexpression increased cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1β/NF-κB p65 signals.
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