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Updated: Jan 16, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment

Published on: April 22, 2019

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Quercetin as a Bitter Taste Receptor Agonist with Anticancer Effects in Head and Neck Cancer Cells

Gavin Turner, Sarah M Sywanycz, Brianna L Hill

    Biorxiv : the Preprint Server for Biology
    |September 26, 2025
    PubMed
    Abstract

    Insights

    Quercetin, a compound found in plants, activates bitter taste receptors (T2Rs) in head and neck squamous cell carcinoma (HNSCC) cells. This activation reduces cancer cell viability and triggers mitochondrial depolarization, suggesting a potential anticancer role for quercetin in HNSCC.

    Area of Science:

    • Oncology
    • Cell Biology
    • Pharmacology

    Background:

    • Quercetin exhibits anticancer properties in preclinical models of head and neck squamous cell carcinoma (HNSCC).
    • Bitter taste receptors (T2Rs) are expressed in HNSCC cells and their activation by bitter compounds like quercetin can induce apoptosis.
    • Increased T2R expression in HNSCC correlates with improved patient survival.

    Purpose of the Study:

    • To investigate quercetin's role as an anticancer T2R agonist in HNSCC cells.
    • To assess the effects of quercetin on calcium (Ca 2+ ) signaling, cell viability, and mitochondrial function in HNSCC.

    Main Methods:

    • Calcium imaging was used to assess quercetin-mediated Ca 2+ responses in HNSCC cell lines, with and without T2R14 antagonist LF1 and G-protein inhibitor YM-254980 (YM).
    • Cell viability was evaluated using crystal violet and MTS assays in cell lines and patient-derived tumor slices.
    • Mitochondrial depolarization was measured using TMRE in the presence and absence of T2R pathway inhibitors.

    Main Results:

    • Quercetin induced a significant Ca 2+ response in HNSCC cells, which was attenuated by LF1 and YM.
    • Quercetin reduced cell viability in vitro and showed a trend towards decreased viability in tumor slices.
    • Quercetin treatment led to mitochondrial depolarization, an effect reduced by LF1 but not YM.

    Conclusions:

    • Quercetin elicits a Ca 2+ response in HNSCC cells, likely mediated by T2R14.
    • Quercetin decreases HNSCC cell viability and induces mitochondrial depolarization.
    • These findings support quercetin's potential as an anticancer agent targeting T2Rs in HNSCC.

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