ArticleScientific reports2020
NF-κB inhibitor with Temozolomide results in significant apoptosis in glioblastoma via the NF-κB(p65) and actin cytoskeleton regulatory pathways.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Challenges in Developing a Microglial NF-Kappa B Conditional Mouse Model for Glioblastoma Studies.Cells · 2026Article
- Actin, connexin-43 and GAP-43 expression in gliomas: real-world associations with IDH status, tumor burden and survival.Journal of neuro-oncology · 2026Article
- Donafenib suppresses glioblastoma progression: potential enhancement of therapeutic response in TMZ-resistant models.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Diphenyl Diselenide and Temozolomide: Downregulation of Inflammatory, Redox, and Tumor-Associated Pathways in Glioblastoma.Biological trace element research · 2026Article
- Decoding Glioblastoma Complexity Through Extracellular Vesicles, Organ-on-Chip Models, and Deep Learning.Cells · 2026Review
- Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.Cancer gene therapy · 2026Review
- Pathophysiological and Etiological Corroborations for the Mechanistic Design of Intranasal Therapies in Glioblastoma Multiforme.Current pharmaceutical design · 2026Review
- Multi-Omics and Single-Cell Dissection of Exostosin Glycosyltransferases (EXT1/EXT2) Reveals Divergent Oncogenic Roles and Therapeutic Vulnerabilities in Gliomas.Journal of Cancer · 2026Article
- Exploration of the Immune Microenvironment of Melanoma and Construction of Prognostic Models Based on the Expression Profile of Lysine Crotonylation-Related Genes.International journal of general medicine · 2026Article
- β-Lapachone sensitizes glioblastoma to Temozolomide by inhibiting NF-κB signaling.Functional & integrative genomics · 2025Article
- Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tenocytes.Molecular biology reports · 2025Article
- Sialylation Inhibition Impairs Migration and Promotes Adhesion of GBM Cells.International journal of molecular sciences · 2025Article
- Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025Review
- Calanquinone A suppresses glioma progression via STAT3-mediated regulation of c-Myc and MMP9.Discover oncology · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- 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
- NF-κB and apoptosis: colorectal cancer progression and novel strategies for treatment.European journal of medical research · 2025Review
- MiR 329/449 Suppresses Cell Proliferation, Migration and Synergistically Sensitizes GBM to TMZ by Inhibiting Src/FAK, NF-kB, and Cyclin D1 Activity.International journal of molecular sciences · 2025Article
- Amino acid metabolism in glioblastoma pathogenesis, immune evasion, and treatment resistance.Cancer cell international · 2025Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most malignant brain tumor characterized by intrinsic or acquired resistance to chemotherapy. GBM tumors show nuclear factor-κB (NF-κB) activity that has been associated with tumor formation, growth, and increased resistance to therapy. We investigated the effect of NF-κB inhibitor BAY 11-7082 with Temozolomide (TMZ) on the signaling pathways in GBM pathogenesis. GBM cells and patient-derived GBM cells cultured in 3D microwells were co-treated with BAY 11-7082 and TMZ or BAY 11-7082 and TMZ alone, and combined experiments of cell proliferation, apoptosis, wound healing assay, as well as reverse-phase protein arrays, western blot and immunofluorescence staining were used to evaluate the effects of drugs on GBM cells. The results revealed that the co-treatment significantly altered cell proliferation by decreasing GBM viability, suppressed NF-κB pathway and enhanced apoptosis. Moreover, it was found that the co-treatment of BAY 11-7082 and TMZ significantly contributed to a decrease in the migration pattern of patient-derived GBM cells by modulating actin cytoskeleton pathway. These findings suggest that in addition to TMZ treatment, NF-κB can be used as a potential target to increase the treatment's outcomes. The drug combination strategy, which is significantly improved by NF-κB inhibitor could be used to better understand the underlying mechanism of GBM pathways in vivo and as a potential therapeutic tool for GBM treatment.
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Registered trials
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