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Real-time Live-cell Flow Cytometry to Investigate Calcium Influx, Pore Formation, and Phagocytosis by P2X7 Receptors in Adult Neural Progenitor Cells
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Published on: April 3, 2019

P2X7 receptor antagonism in the treatment of cancers

Sébastien Roger, Pablo Pelegrin

    Expert Opinion on Investigational Drugs
    |May 31, 2011
    PubMed

    Insights

    Extracellular ATP-gated P2X7 receptors are involved in both inflammation and cancer. Targeting these P2X7 receptors may offer new strategies for treating inflammatory diseases and reducing cancer metastasis.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Immunology

    Background:

    • P2X7 receptors are ATP-gated ion channels found on immune and epithelial cells.
    • Their activation in immune cells triggers pro-inflammatory cytokine release, making them targets for inflammatory disease treatment.
    • Recent findings show P2X7 receptor expression in various tumors, suggesting potential as cancer biomarkers.

    Discussion:

    • Tumor cells exhibit dual responses to extracellular ATP via P2X7 signaling: downregulating receptors to evade apoptosis or utilizing them for survival and invasion.
    • High extracellular ATP in tumors can act as a stressor, initiating P2X7-mediated cell death.
    • Enhanced P2X7-dependent invasiveness may represent a cancer cell escape mechanism from high ATP environments.

    Key Insights:

    • P2X7 receptors play a complex role in cancer, influencing both cell death evasion and promoting invasion.
    • Extracellular ATP levels in tumors can paradoxically trigger cell death or promote survival and metastasis via P2X7.
    • P2X7 receptor antagonists present a novel therapeutic avenue for combating cancer metastasis.

    Outlook:

    • Further research into P2X7 receptor function in different cancer types is warranted.
    • Developing specific P2X7 antagonists could enhance conventional cancer therapies.
    • Understanding the dual role of P2X7 in cancer may lead to targeted therapeutic strategies.

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