ArticleNeuro-oncology2025
Targeting PGE2 mediated senescent neuron improves tumor therapy.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Spatial anchoring of lipid metabolism shapes immune fate in the tumor microenvironment.Lipids in health and disease · 2026Review
- Mechanistic evaluation of pachymic acid in breast cancer via network pharmacology and in vitro validation.BMC complementary medicine and therapies · 2026Article
- Organoids as next-generation models for investigating intracranial tumours.Molecular brain · 2026Review
- The role of lipid metabolism in neuronal senescence.FEBS open bio · 2026Review
- Targeting inflammatory microenvironments: overcoming therapy resistance and immunosuppression.Molecular cancer · 2026Review
- Review
- Machine learning integration with multi-omics data constructs a robust prognostic model and identifies PTGES3 as a therapeutic target for precision oncology in lung adenocarcinoma.Frontiers in immunology · 2025Article
- Prostaglandin EEXCLI journal · 2025Review
- Inhibition of Cyclin-dependent Kinase Counteracts Neuron-promoted Bladder and Endometrial Tumorigenesis: A Systematic Analysis.In vivo (Athens, Greece)Article
- Beyond the Poly(A) Tail: The Expanding Functional Landscape of PABPN1 and Its Dysregulation in OPMD and Cancer.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
15 authors.
Funding
Abstract
backgroundRecent studies have highlighted bidirectional signaling between tumors and neurons; however, the interactions between tumors and neurons in response to radio-/chemotherapy remain obscure, which hampers the tumor treatment.
methodsGlioblastoma organoids (GBOs) and primary neuron coculture, targeted metabonomics, RNA pulldown, mass spectrum, co-immunoprecipitation, RNA-sequencing, transcript/protein validations, and multi-electrode arrays were performed to analyze neuron-tumor interaction in response to therapy. In vivo validations were conducted in orthotopic mouse models. Diagnostic and prognostic values were evaluated in serum, tissue microarray as well as The Cancer Genome Atlas (TCGA).
resultsGBOs recruited and induced pro-tumor-survival senescent neurons upon radiation/chemotherapeutic treatment. Targeted metabonomics revealed that significantly increased tumor-derived prostaglandin E2 (PGE2) induced neuronal senescence phenotype. Screening of enzymes involved in PGE2 synthesis identified prostaglandin E synthase 3 (PTGES3) as the key enzyme responsible for PGE2 upregulation. Biochemical studies revealed that irradiation or chemotherapeutic drug-triggered asparagine endopeptidase (AEP) specifically cleaved eukaryotic translation initiation factor 4A1 (eIF4A1) to produce truncated C-terminal eIF4A1 (teIF4A1-C), which dissociated from DEAD-box helicase 6 (DDX6) and recruited eIF4A3 and polyadenylate-binding protein nuclear 1 (PABPN1) to promote the mRNA stability of PTGES3. Elevated PGE2 reciprocally enhanced AEP expression. Inhibiting PGE2 or AEP reduced neuronal senescence and delayed tumor progression. Strikingly, single-cell analysis further showed that expressions of AEP/PTGES3/EIF4A1 in tumor cells were consistent with senescent neuronal cyclin-dependent kinase inhibitor 1A (CDKN1A) in high-neuronal-connectivity glioblastoma. The serum PGE2 concentration was elevated after radiation and higher in resistant glioblastoma patients. High expression of PTGES3 was associated with a poor prognosis.
conclusionsOur study revealed that the AEP/PGE2 feedback loop modulates tumor-induced neuronal senescence upon radio-/chemotherapy and highlights the therapeutic value to improve tumor therapy.
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