ArticleNeuro-oncology2008
Tumor-growth-promoting cyclooxygenase-2 prostaglandin E2 pathway provides medulloblastoma therapeutic targets.
Article in Neuro-oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 79 citations in OpenAlex.
- Targeting the COX-2/PGECancer immunology, immunotherapy : CII · 2026Review
- Celecoxib Inhibits Vasculogenic Mimicry and Induces Apoptosis in the D17 Canine Osteosarcoma Cell Line via the COX-2/PGE2 Signaling Axis.Veterinary sciences · 2026Article
- Viral transformation of stem cells into cancer stem cells and tumor enhancement by immunoexcito-oncomodulation: Accumulating evidence that most cancers are virally induced and further altered to increase their aggressiveness.Surgical neurology international · 2026Article
- Investigation of the Effects of Polyunsaturated Fatty Acid Ratios in Human SH-SY5Y Cells byTurkish journal of pharmaceutical sciences · 2025Article
- The roles of COX-2 in protozoan infection.Frontiers in immunology · 2023Review
- Global metabolomics study on the pathogenesis of pediatric medulloblastoma via UPLC- Q/E-MS/MS.PloS one · 2023Article
- Targeting Angiogenic Factors for the Treatment of Medulloblastoma.Current treatment options in oncology · 2022Review
- Prostaglandin Pathways: Opportunities for Cancer Prevention and Therapy.Cancer research · 2022Review
- Immunosuppression in Medulloblastoma: Insights into Cancer Immunity and Immunotherapy.Current treatment options in oncology · 2021Review
- Cytomegalovirus DNA in non-glioblastoma multiforme brain tumors of infants.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- Medulloblastoma drugs in development: Current leads, trials and drawbacks.European journal of medicinal chemistry · 2021Review
- Drug Repurposing in Medulloblastoma: Challenges and Recommendations.Current treatment options in oncology · 2020Review
- Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid.Cancers · 2020Article
- Immunotherapy for Medulloblastoma: Current Perspectives.ImmunoTargets and therapy · 2020Review
- Inhibition of Microsomal Prostaglandin E Synthase-1 in Cancer-Associated Fibroblasts Suppresses Neuroblastoma Tumor Growth.EBioMedicine · 2018Article
- Establishment and characterization of an orthotopic patient-derived Group 3 medulloblastoma model for preclinical drug evaluation.Scientific reports · 2017Article
- Role of Cyclooxygenase-2 Pathway in Creating an Immunosuppressive Microenvironment and in Initiation and Progression of Wilms' Tumor.Neoplasia (New York, N.Y.) · 2017Article
- Wnt/β-catenin pathway regulates MGMT gene expression in cancer and inhibition of Wnt signalling prevents chemoresistance.Nature communications · 2015Article
- A standardized and reproducible protocol for serum-free monolayer culturing of primary paediatric brain tumours to be utilized for therapeutic assays.Scientific reports · 2015Article
- COX/mPGES-1/PGE2 pathway depicts an inflammatory-dependent high-risk neuroblastoma subset.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E(2) (PGE(2)) has been shown to play important roles in several aspects of tumor development and progression. PGE(2) is synthesized from arachidonic acid by cyclooxygenases (COX) and prostaglandin E synthases (PGES) and mediates its biological activity through binding to the four prostanoid receptors EP(1) through EP(4). In this study, we show for the first time that medulloblastoma (MB), the most common malignant childhood brain tumor, expresses high levels of COX-2, microsomal prostaglandin E synthase-1, and EP(1) through EP(4) and secretes PGE(2). PGE(2) and the EP(2) receptor agonist butaprost stimulated MB cell proliferation. Treatment of MB cells with COX inhibitors suppressed PGE(2) production and induced caspase-dependent apoptosis. Similarly, specific COX-2 silencing by small interfering RNA inhibited MB cell growth. EP(1) and EP(3) receptor antagonists ONO-8713 and ONO-AE3-240, but not the EP(4) antagonists ONO-AE3-208 and AH 23848, inhibited tumor cell proliferation, indicating the significance of EP(1) and EP(3) but not EP(4) for MB growth. Administration of COX inhibitors at clinically achievable nontoxic concentrations significantly inhibited growth of established human MB xenografts. Apoptosis was increased, proliferation was reduced, and angiogenesis was inhibited in MBs treated with COX inhibitors. This study suggests that PGE(2) is important for MB growth and that therapies targeting the prostanoid metabolic pathway are potentially beneficial and should be tested in clinical settings for treatment of children with MB.
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