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Updated: Mar 30, 2026

Three-Dimensional 3D Tumor Spheroid Invasion Assay
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Three-Dimensional 3D Tumor Spheroid Invasion Assay

Published on: May 1, 2015

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Tumor growth suppression by inhibiting both autophagy and STAT3 signaling in HNSCC

Teng-Fei Fan, Lin-Lin Bu, Wei-Ming Wang

    Oncotarget
    |November 13, 2015
    PubMed

    Insights

    Autophagy acts as a double-edged sword in head and neck squamous cell carcinoma (HNSCC). Inhibiting signal transducer and activator of transcription 3 (STAT3) and autophagy together shows promise for HNSCC treatment.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Cellular Biology

    Background:

    • Autophagy's role in cancer is complex, acting as both a tumor suppressor and promoter.
    • The precise mechanisms linking autophagy to tumorigenesis, particularly in head and neck squamous cell carcinoma (HNSCC), remain unclear.
    • Signal transducer and activator of transcription 3 (STAT3) is implicated in cancer progression, but its interplay with autophagy in HNSCC requires elucidation.

    Purpose of the Study:

    • To investigate the relationship between signal transducer and activator of transcription 3 (STAT3) phosphorylation and autophagy in human head and neck squamous cell carcinoma (HNSCC).
    • To explore the therapeutic potential of combined STAT3 and autophagy inhibition in HNSCC treatment.

    Main Methods:

    • Analysis of the correlation between decreased p-STAT3 levels and increased autophagy via Akt/mTOR and Erk pathways in HNSCC.
    • Utilizing a STAT3 inhibitor (NSC748859) to assess its effects on apoptosis and autophagy.
    • Evaluating the impact of pharmacological or genetic inhibition of autophagy and STAT3 on HNSCC cell apoptosis.
    • Assessing the combined efficacy of STAT3 inhibition and autophagy suppression in a xenograft HNSCC model.

    Main Results:

    • Decreased STAT3 phosphorylation correlated with increased autophagy in HNSCC, mediated by Akt/mTOR and Erk signaling.
    • STAT3 inhibition by NSC74859 induced apoptosis and autophagy, with autophagy subsequently inhibiting apoptosis.
    • Combined inhibition of STAT3 and autophagy sensitized HNSCC cells to apoptosis.
    • Simultaneous suppression of STAT3 and autophagy demonstrated superior tumor regression in a xenograft model compared to single treatments.

    Conclusions:

    • Autophagy plays a role in alleviating apoptotic cell death in HNSCC.
    • Combined inhibition of STAT3 (using NSC74859) and autophagy presents a potential novel therapeutic strategy for HNSCC.
    • Targeting both STAT3 and autophagy pathways offers a promising approach for enhancing HNSCC treatment efficacy.
    Keywords:
    STAT3apoptosisautophagyhead and neck cancer

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