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    Inhibition of purinergic P2X receptor 7 (P2X7R) decreases granulocyte-macrophage colony-stimulating factor (GM-CSF) expression in U251 glioblastoma cells

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    Author
    Drill, M; Powell, KL; Kan, LK; Jones, NC; O'Brien, TJ; Hamilton, JA; Monif, M
    Date
    2020-09-09
    Source Title
    Scientific Reports
    Publisher
    NATURE RESEARCH
    University of Melbourne Author/s
    Powell, Kim; Monif, Mastura; Hamilton, John; O'Brien, Terence; Jones, Nigel
    Affiliation
    Medicine and Radiology
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Drill, M., Powell, K. L., Kan, L. K., Jones, N. C., O'Brien, T. J., Hamilton, J. A. & Monif, M. (2020). Inhibition of purinergic P2X receptor 7 (P2X7R) decreases granulocyte-macrophage colony-stimulating factor (GM-CSF) expression in U251 glioblastoma cells. SCIENTIFIC REPORTS, 10 (1), https://doi.org/10.1038/s41598-020-71887-x.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251571
    DOI
    10.1038/s41598-020-71887-x
    Abstract
    Glioblastoma is the most aggressive form of primary brain cancer, with a median survival of 12-15 months. The P2X receptor 7 (P2X7R) is upregulated in glioblastoma and is associated with increased tumor cell proliferation. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) is also upregulated in glioblastoma and has been shown to have both pro- and anti-tumor functions. This study investigates the potential mechanism linking P2X7R and GM-CSF in the U251 glioblastoma cell line and the therapeutic potential of P2X7R antagonism in this setting. P2X7R protein and mRNA was demonstrated to be expressed in the U251 cell line as assessed by immunocytochemistry and qPCR. Its channel function was intact as demonstrated by live cell confocal imaging using a calcium indicator Fluo-4 AM. Inhibition of P2X7R using antagonist AZ10606120, decreased both GM-CSF mRNA (P < 0.05) and protein (P < 0.01) measured by qPCR and ELISA respectively. Neutralization of GM-CSF with an anti-GM-CSF antibody did not alter U251 cell proliferation, however, P2X7R antagonism with AZ10606120 significantly reduced U251 glioblastoma cell numbers (P < 0.01). This study describes a novel link between P2X7R activity and GM-CSF expression in a human glioblastoma cell line and highlights the potential therapeutic benefit of P2X7R inhibition with AZ10606120 in glioblastoma.

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