ArticleOncogene2015
Disruption of prion protein-HOP engagement impairs glioblastoma growth and cognitive decline and improves overall survival.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Stress-inducible phosphoprotein 1 (STIP1) is a critical stemness regulator in mouse embryonic stem cells and early mammalian development.Communications biology · 2025Article
- Re-evaluation of the relationship between PrPc expression and patient prognosis in primary esophageal squamous cell carcinoma and primary hepatocellular carcinoma.Scientific reports · 2024Article
- The expression of pro-prion, a transmembrane isoform of the prion protein, leads to the constitutive activation of the canonical Wnt/β-catenin pathway to sustain the stem-like phenotype of human glioblastoma cells.Cancer cell international · 2024Article
- Prion protein regulates invasiveness in glioblastoma stem cells.BMC cancer · 2024Article
- The Humanization and Maturation of an Anti-PrPc Antibody.Bioengineering (Basel, Switzerland) · 2024Article
- Integrated transcriptomics uncovers an enhanced association between the prion protein gene expression and vesicle dynamics signatures in glioblastomas.BMC cancer · 2024Article
- Roles of prion proteins in mammalian development.Animal cells and systems · 2024Review
- Emerging roles of the cellular prion protein (PrPCellular and molecular life sciences : CMLS · 2023Review
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Melatonin and 5-fluorouracil combination chemotherapy: opportunities and efficacy in cancer therapy.Cell communication and signaling : CCS · 2023Review
- The Role of Cellular Prion Protein in Glioma Tumorigenesis Could Be through the Autophagic Mechanisms: A Narrative Review.International journal of molecular sciences · 2023Review
- Article
- High Expression ofCancers · 2022Article
- Unconventional Protein Secretion in Brain Tumors Biology: Enlightening the Mechanisms for Tumor Survival and Progression.Frontiers in cell and developmental biology · 2022Review
- Identification and analysis of a prognostic ferroptosis and iron-metabolism signature for esophageal squamous cell carcinoma.Journal of Cancer · 2022Article
- Detailing the ultrastructure's increase of prion protein in pancreatic adenocarcinoma.World journal of gastroenterology · 2021Article
- The Cellular Prion Protein and the Hallmarks of Cancer.Cancers · 2021Review
- MT1 and MT2 melatonin receptors play opposite roles in brain cancer progression.Journal of molecular medicine (Berlin, Germany) · 2021Article
- The Role of Cellular Prion Protein in Promoting Stemness and Differentiation in Cancer.Cancers · 2021Review
- The Role of Cellular Prion Protein in Cancer Biology: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas (GBMs) are resistant to current therapy protocols and identification of molecules that target these tumors is crucial. Interaction of secreted heat-shock protein 70 (Hsp70)-Hsp90-organizing protein (HOP) with cellular prion protein (PrP(C)) triggers a large number of trophic effects in the nervous system. We found that both PrP(C) and HOP are highly expressed in human GBM samples relative to non-tumoral tissue or astrocytoma grades I-III. High levels of PrP(C) and HOP were associated with greater GBM proliferation and lower patient survival. HOP-PrP(C) binding increased GBM proliferation in vitro via phosphatidylinositide 3-kinase and extracellular-signal-regulated kinase pathways, and a HOP peptide mimicking the PrP(C) binding site (HOP230-245) abrogates this effect. PrP(C) knockdown impaired tumor growth and increased survival of mice with tumors. In mice, intratumor delivery of HOP230-245 peptide impaired proliferation and promoted apoptosis of GBM cells. In addition, treatment with HOP230-245 peptide inhibited tumor growth, maintained cognitive performance and improved survival. Thus, together, the present results indicate that interfering with PrP(C)-HOP engagement is a promising approach for GBM therapy.
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Registered trials
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