ArticleCancer letters2019
The Ig superfamily protein PTGFRN coordinates survival signaling in glioblastoma multiforme.
Article in Cancer letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 42 citations in OpenAlex.
- Pan-cancer analysis reveals the oncogenic and immunomodulatory roles of PTGFRN across human cancers.Scientific reports · 2026Article
- Bioengineering of extracellular vesicles with scaffold proteins for drug delivery.Journal of nanobiotechnology · 2026Review
- Polyamine acetylation mediates crosstalk between cancer cells and myeloid cells to promote mesenchymal/plurimetabolic states in glioblastoma.Neuro-oncology · 2025Article
- 8C7: A Fully Human Anti-PTGFRN Monoclonal Antibody-Drug Conjugate Inhibiting Tumour Growth of Mesothelioma and Paediatric Medulloblastoma Cell Lines.Journal of cellular and molecular medicine · 2025Article
- Prostaglandin F2 receptor negative regulator as a potential target for chimeric antigen receptor-T cell therapy for glioblastoma.Cancer immunology, immunotherapy : CII · 2025Article
- Article
- Effect of PTFGRN Expression on the Proteomic Profile of A431 Cells and Determination of the PTGFRN Interactome.ACS omega · 2024Article
- Molecular subtypes based on PANoptosis-related genes and tumor microenvironment infiltration characteristics in lower-grade glioma.Functional & integrative genomics · 2023Review
- Review
- Acquisition of Immune Privilege in GBM Tumors: Role of Prostaglandins and Bile Salts.International journal of molecular sciences · 2023Article
- Immune microenvironment analysis and novel biomarkers of early-stage lung adenocarcinoma evolution.Frontiers in oncology · 2023Article
- Cryo-electron Microscopic Analysis of Single-Pass Transmembrane Receptors.Chemical reviews · 2022Review
- Integrative analysis of cell adhesion molecules in glioblastoma identified prostaglandin F2 receptor inhibitor (PTGFRN) as an essential gene.BMC cancer · 2022Review
- Genome-wide promoter methylation profiling in a cellular model of melanoma progression reveals markers of malignancy and metastasis that predict melanoma survival.Clinical epigenetics · 2022Article
- Article
- A New Hypoxia-Related Prognostic Risk Score (HPRS) Model Was Developed to Indicate Prognosis and Response to Immunotherapy for Lung Adenocarcinoma.Journal of oncology · 2022Article
- Bench to bedside radiosensitizer development strategy for newly diagnosed glioblastoma.Radiation oncology (London, England) · 2021Review
- Article
- Surfaceome Proteomic of Glioblastoma Revealed Potential Targets for Immunotherapy.Frontiers in immunology · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) is the most malignant primary brain tumor with a median survival of approximately 14 months. Despite aggressive treatment of surgical resection, chemotherapy and radiation therapy, only 3-5% of GBM patients survive more than 3 years. Contributing to this poor therapeutic response, it is believed that GBM contains both intrinsic and acquired mechanisms of resistance, including resistance to radiation therapy. In order to define novel mediators of radiation resistance, we conducted a functional knockdown screen, and identified the immunoglobulin superfamily protein, PTGFRN. In GBM, PTGFRN is found to be overexpressed and to correlate with poor survival. Reducing PTGFRN expression radiosensitizes GBM cells and potently decreases the rate of cell proliferation and tumor growth. Further, PTGFRN inhibition results in significant reduction of PI3K p110β and phosphorylated AKT, due to instability of p110β. Additionally, PTGFRN inhibition decreases nuclear p110β leading to decreased DNA damage sensing and DNA damage repair. Therefore overexpression of PTGFRN in glioblastoma promotes AKT-driven survival signaling and tumor growth, as well as increased DNA repair signaling. These findings suggest PTGFRN is a potential signaling hub for aggressiveness in GBM.
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Identifiers
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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 Socratic graph.