ArticleScientific reports2024
Temozolomide promotes matrix metalloproteinase 9 expression through p38 MAPK and JNK pathways in glioblastoma cells.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Methyl 4-O-Demethylbarbatate Destabilises HIF-1α and Enhances Temozolomide Sensitivity in Glioma Cells.Cell proliferation · 2026Article
- Gene expression profiling enables refined parcellation of cortical layers in the heterogeneous human cerebral cortex.Genome medicine · 2026Article
- Forming a Precise and Reproducible Hypoxic Tumor Microenvironment in Glioblastoma by High Cell Density Bioprinting.Advanced healthcare materials · 2026Article
- Diphenyl Diselenide and Temozolomide: Downregulation of Inflammatory, Redox, and Tumor-Associated Pathways in Glioblastoma.Biological trace element research · 2026Article
- Novel CAR T cell blend targeting PDPN and GD2 to overcome glioblastoma heterogeneity.Journal for immunotherapy of cancer · 2026Article
- Deep learning for predicting patient drug response by transferring gene-level and cell-level knowledge to tumors.NPJ precision oncology · 2026Article
- Review
- Exploring the Interactive Effect of Pectins fromACS omega · 2026Article
- Novel cilengitide derivatives suppress migration and invasion of temozolomide-resistant glioblastoma cells via MAPK/Akt pathway inhibition.Journal of neuro-oncology · 2026Article
- Molecular Signatures and Network Alterations Underlying GBM Progression and Recurrence.Medicina (Kaunas, Lithuania) · 2026Article
- Role of matrix metalloproteinases in the invasion of glioblastoma and drug interventions (Review).International journal of molecular medicine · 2026Review
- Reconstructing the glioblastoma microenvironment in heterotypic 3D spheroids: a multicellular model to study tumor-stromal crosstalk.Frontiers in bioengineering and biotechnology · 2026Article
- Combinatorial effect of epirubicin and 5-fluorouracil in the treatment of temozolomide-resistant glioblastoma cells.Turkish journal of biology = Turk biyoloji dergisi · 2026Article
- Network-driven prioritization and functional phenotyping nominate TTC23 as a biomarker-informed target in chlorpromazine repurposing for glioblastoma.Frontiers in pharmacology · 2026Article
- Cyclooxygenase-2 as a potential therapeutic target in the treatment of chemoresistant glioblastomas.Medical oncology (Northwood, London, England) · 2025Review
- Engineered N-TIMP2 Variant Specifically Targeting MMP-9 Exhibits Potent Anti-Glioblastoma Activity.Biomolecules · 2025Article
- Calanquinone A suppresses glioma progression via STAT3-mediated regulation of c-Myc and MMP9.Discover oncology · 2025Article
- Matrix Metalloproteinases in Glioma: Drivers of Invasion and Therapeutic Targets.Biotech (Basel (Switzerland)) · 2025Review
- High intra-tumoral and serum matrix metalloproteinase 9 levels are associated with reduced survival of patients with glioblastoma and brain metastases.Frontiers in oncology · 2025Article
- The effect of travoprost on primary human limbal epithelial cells and the siRNA-based aniridia limbal epithelial cell model, in vitro.PloS one · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Glioblastoma (GBM) is a highly aggressive and deadly brain cancer. Temozolomide (TMZ) is the standard chemotherapeutic agent for GBM, but the majority of patients experience recurrence and invasion of tumor cells. We investigated whether TMZ treatment of GBM cells regulates matrix metalloproteinases (MMPs), which have the main function to promote tumor cell invasion. TMZ effectively killed GL261, U343, and U87MG cells at a concentration of 500 µM, and surviving cells upregulated MMP9 expression and its activity but not those of MMP2. TMZ also elevated levels of MMP9 mRNA and MMP9 promoter activity. Subcutaneous graft tumors survived from TMZ treatment also exhibited increased expression of MMP9 and enhanced gelatinolytic activity. TMZ-mediated MMP9 upregulation was specifically mediated through the phosphorylation of p38 and JNK. This then stimulates AP-1 activity through the upregulation of c-Fos and c-Jun. Inhibition of the p38, JNK, or both pathways counteracted the TMZ-induced upregulation of MMP9 and AP-1. This study proposes a potential adverse effect of TMZ treatment for GBM: upregulation of MMP9 expression potentially associated with increased invasion and poor prognosis. This study also provides valuable insights into the molecular mechanisms by which TMZ treatment leads to increased MMP9 expression in GBM cells.
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