ArticleScience advances2016
Targeting NF-κB in glioblastoma: A therapeutic approach.
Article in Science advances, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 138 citations in OpenAlex.
- Melatonin enhances radiofrequency-induced NK antitumor immunity, causing cancer metabolism reprogramming and inhibition of multiple pulmonary tumor development.Signal transduction and targeted therapy · 2021Trial
- Myrtenol modulates TWEAK/TLR4-NF-κB, miR-21, PTEN, and ERK-1 expressions and improves behavioral outcomes in a rat glioblastoma model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Dietary Polyphenols as Natural Modulators of NF-κB Signaling in Inflammation-Driven Non-Communicable Diseases: Focus on Cancer.Food science & nutrition · 2026Review
- Redox-sensitive and inflammatory pathway modulation by Chrysin confers protection against aflatoxin B1-induced hepato-renal damage.Mycotoxin research · 2026Article
- Article
- Advancements in Drug Delivery Systems in Glioblastoma Therapy.International journal of molecular sciences · 2026Review
- Therapeutic Potential of NF-κB Inhibition in Glioblastoma: Gene Therapy Approach with rAAV-5 Mediated IκBαM Overexpression.Molecular biotechnology · 2026Article
- BRD2 bromodomain-mediated regulation of cell state plasticity modulates therapy response in glioblastoma.Neuro-oncology · 2025Article
- Molecular characterization of macrophage-related prognostic factors in glioblastoma revealed by combined analysis on single-cell and bulk transcriptome data.Discover oncology · 2025Article
- Immune factors and their role in tumor aggressiveness in glioblastoma: Atypical cadherin FAT1 as a promising target for combating immune evasion.Cellular & molecular biology letters · 2025Review
- Recent Advances in Therapeutic Peptides: Innovations and Applications in Treating Infections and Diseases.ACS omega · 2025Review
- Assessing the diagnostic, prognostic, and therapeutic potential of the somatostatin/cortistatin system in glioblastoma.Cellular and molecular life sciences : CMLS · 2025Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Expression of toll-like receptors and inflammatory mediators in primary human glioma cells (low- and high-grade) compared to primary cells from epileptic human brain.Iranian journal of basic medical sciences · 2025Article
- Biological Activity of Natural and Synthetic Peptides as Anticancer Agents.International journal of molecular sciences · 2024Review
- Review
- IFI35 regulates non-canonical NF-κB signaling to maintain glioblastoma stem cells and recruit tumor-associated macrophages.Cell death and differentiation · 2024Article
- Overcoming Resistance to Temozolomide in Glioblastoma: A Scoping Review of Preclinical and Clinical Data.Life (Basel, Switzerland) · 2024Article
- Joint multi-omics discriminant analysis with consistent representation learning using PANDA.Research square · 2024Article
- Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Glioblastoma multiforme (GBM) is the most common and lethal form of intracranial tumor. We have established a lentivirus-induced mouse model of malignant gliomas, which faithfully captures the pathophysiology and molecular signature of mesenchymal human GBM. RNA-Seq analysis of these tumors revealed high nuclear factor κB (NF-κB) activation showing enrichment of known NF-κB target genes. Inhibition of NF-κB by either depletion of IκB kinase 2 (IKK2), expression of a IκBαM super repressor, or using a NEMO (NF-κB essential modifier)-binding domain (NBD) peptide in tumor-derived cell lines attenuated tumor proliferation and prolonged mouse survival. Timp1, one of the NF-κB target genes significantly up-regulated in GBM, was identified to play a role in tumor proliferation and growth. Inhibition of NF-κB activity or silencing of Timp1 resulted in slower tumor growth in both mouse and human GBM models. Our results suggest that inhibition of NF-κB activity or targeting of inducible NF-κB genes is an attractive therapeutic approach for GBM.
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What OpenQuestion holds
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.