ArticlePloS one2025
Purinergic P2X receptor 7 (P2X7R) inhibition induced cytotoxicity in glioblastoma.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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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
2 citing papers in PubMed.
- Effects on mouse melanoma and immune cells of P2X7 receptor positive allosterism by clemastine.Purinergic signalling · 2026Article
- Metabolism and Immunity-Adapted Radiotherapy (M.I.A.R): A Conceptual Framework for Overcoming the Therapeutic Plateau in Clinical Radiotherapy.Current oncology (Toronto, Ont.) · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common and aggressive form of primary brain cancer with a median survival of 15 months from diagnosis. The purinergic receptor P2X7 (P2X7R) is a regulator of several cell signalling pathways, and its expression is upregulated in glioblastoma. This study examined the expression and function of P2X7R in a human glioblastoma cell line, U251. We used a pharmacological antagonist of P2X7R, AZ10606120, to inhibit receptor function and delineate downstream consequences of receptor inhibition. Using RNA sequencing we demonstrated that P2X7R was expressed in the U251 cell line, harbouring both Y155H (Tyr to His) and E496A (Glu to Ala) single nucleotide polymorphism (SNP) mutations. The receptors functionality - namely its pore and channel conductance states were intact. Inhibition of P2X7R with small molecule antagonist AZ10606120, for 72 hours significantly decreased U251 cell number (p < 0.0001), and significantly increased tumour cell death, as evidenced by increased LDH release (p < 0.001). This reduction in tumour cell number was concentration-dependent, modelled by a least squares linear regression (R2 = 0.8221, IC50 = 17µM). The primary mode of cell death induced by AZ10606120 was shown to not be apoptosis, demonstrated through no significant changes in annexin V or cleaved caspase 3 staining in AZ10606120 treated cell versus control cells. Multiplex mRNA analysis demonstrated changes in genes associated with both apoptosis and pyroptosis, whilst a decrease in receptor-interacting serine/threonine-protein kinase 1 (RIPK1) expression along with an increase in TNFR1-associated death domain protein (TRADD) expression suggests potential involvement of the TRADD mediated RIPK1-independent necroptosis pathway. Collectively, this study describes several key characteristics of AZ10606120s acting as an anti-tumour small molecule pharmaceutical and highlights the potential of P2X7R inhibition as a novel therapeutic target in glioblastoma.
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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.