ArticleJournal of neuro-oncology2007
Aberrant constitutive activation of nuclear factor kappaB in glioblastoma multiforme drives invasive phenotype.
Article in Journal of neuro-oncology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 115 citations in OpenAlex.
- Endogenous inhibitors of PP2A activate oncogenic and DNA damage response kinases in glioblastoma.Cancer letters · 2026Article
- Crossroads of cell fate: miR-34-mediated regulation of apoptosis and autophagy in glioblastoma.Discover oncology · 2025Review
- Is Fluoride Blameless?-The Influence of Fluorine Compounds on the Invasiveness of the Human Glioma-like Cell Line U-87.International journal of molecular sciences · 2024Article
- Article
- Targeting NF-κB signaling cascades of glioblastoma by a natural benzophenone, garcinol, viaFrontiers in chemistry · 2024Article
- Blockage of EGFR/AKT and mevalonate pathways synergize the antitumor effect of temozolomide by reprogramming energy metabolism in glioblastoma.Cancer communications (London, England) · 2023Article
- Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma.Journal of clinical medicine · 2023Article
- Transcriptional induction of NF-κB-inducing kinase by E2F4/5 facilitates collective invasion of GBM cells.Scientific reports · 2023Article
- Transcriptional Induction of NF-kB-Inducing Kinase by E2F4/5 Facilitates Collective Invasion of Glioma Cells.Research square · 2023Article
- Fluoride in the Central Nervous System and Its Potential Influence on the Development and Invasiveness of Brain Tumours-A Research Hypothesis.International journal of molecular sciences · 2023Review
- Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO.Oncogene · 2022Article
- ADAR3 activates NF-κB signaling and promotes glioblastoma cell resistance to temozolomide.Scientific reports · 2022Article
- EGFR ligand shifts the role of EGFR from oncogene to tumour suppressor in EGFR-amplified glioblastoma by suppressing invasion through BIN3 upregulation.Nature cell biology · 2022Article
- An NF-κB- and Therapy-Related Regulatory Network in Glioma: A Potential Mechanism of Action for Natural Antiglioma Agents.Biomedicines · 2022Article
- Anti-cancer peptide-based therapeutic strategies in solid tumors.Cellular & molecular biology letters · 2022Article
- Mechanisms of Cell Cycle Arrest and Apoptosis in Glioblastoma.Biomedicines · 2022Review
- NF-κB in neurodegenerative diseases: Recent evidence from human genetics.Frontiers in molecular neuroscience · 2022Review
- Anticancer Mechanism of Curcumin on Human Glioblastoma.Nutrients · 2021Review
- TRIM22 activates NF-κB signaling in glioblastoma by accelerating the degradation of IκBα.Cell death and differentiation · 2021Article
- NF-кB inhibition by DHMEQ: in vitro antiproliferative effects on pilocytic astrocytoma and concise review of the current literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020Article
7 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several recent studies have shown that aberrant constitutive activation of nuclear factor kappaB (NF-kappaB) is present in a variety of cancers including gliomas. NF-kappaB is known to play important roles in the physiological regulation of diverse cellular processes such as inflammation, growth and immunity. In contrast, aberrant activation of this latent transcription factor promotes cancer cell migration, invasion and resistance to chemotherapy. Here we show by electro-mobility shift assay (EMSA) and immuno-staining that constitutive NF-kappaB activation is present in various malignant glioma cell lines as well as in primary cultures derived from tumor tissue. This activation was not serum dependent and it led to high IL-8 gene transcription and protein production. Over-expression of an I-kappaB super-repressor (I-kappaB SR) transgene completely blocked constitutive NF-kappaB activation, nuclear localization and transcription of some but not all NF-kappaB regulated genes indicating that NF-kappaB signaling in glioma cells is I-kappaB dependent. Surprisingly, over-expression of IkappaBSR did not have any effect on the transcription levels of anti-apoptotic genes in these glioma cultures and cell lines. Down-regulation of NF-kappaB activation reduced invasion of glioma cells through matrigel. Collectively these data suggest that aberrant constitutive activation of NF-kappaB in glioblastoma cells promotes their invasive phenotype. Interruption of this aberrant NF-kappaB activity may help reduce the spread of this infiltrative tumor.
Indexed as
Identifiers
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.