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Induction and Validation of Cellular Senescence in Primary Human Cells
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Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

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Sodium butyrate induces cellular senescence in neuroblastoma and prostate cancer cells

Viola Lorenz, Wiebke Hessenkemper, Julia Rödiger

    Hormone Molecular Biology and Clinical Investigation
    |May 12, 2015
    PubMed

    Insights

    Histone deacetylase (HDAC) inhibitors like sodium butyrate (NaBu) induce cellular senescence, a cell division arrest, in cancer cells. This epigenetic regulation, linked to reactive oxygen species (ROS), offers a promising avenue for tumor suppression.

    Area of Science:

    • Epigenetics
    • Cancer Biology
    • Cellular Senescence

    Background:

    • Cellular senescence irreversibly blocks cell division, a valuable mechanism for cancer treatment.
    • Histone deacetylases (HDACs) are key therapeutic targets in oncology, with HDAC inhibitors showing promise in clinical trials.
    • Understanding novel inducers of senescence is crucial for developing new anti-cancer strategies.

    Purpose of the Study:

    • To investigate whether sodium butyrate (NaBu), a class I and II HDAC inhibitor, induces cellular senescence in neuroblastoma and prostate cancer (PCa) cell lines.
    • To explore the effects of other HDAC inhibitors, including a SIRT1 inhibitor, on tumor cell senescence.
    • To elucidate the molecular mechanisms underlying HDAC inhibitor-induced senescence, focusing on gene expression and reactive oxygen species (ROS) production.

    Main Methods:

    • Treatment of neuroblastoma and human prostate cancer cell lines (androgen-dependent and independent) with HDAC inhibitors (NaBu, valproic acid (VPA), and a SIRT1 inhibitor).
    • Assessment of cellular senescence markers, including Senescence-Associated β-galactosidase (SA-β-Gal) and Senescence-Associated Heterochromatin Foci (SAHF).
    • Analysis of mRNA levels for proto-oncogenes (c-Myc, Cyclin D1, E2F1), cell cycle inhibitors (p16), and tumor suppressors (p21).
    • Measurement of reactive oxygen species (ROS) levels following NaBu treatment.

    Main Results:

    • Both NaBu and VPA, HDAC inhibitors, effectively induced cellular senescence in tested tumor cell lines.
    • A SIRT1 inhibitor also triggered cellular senescence, indicating a role for class III HDACs.
    • Senescence markers (SA-β-Gal, SAHF) were expressed in neuroblastoma and prostate cancer cells.
    • NaBu downregulated c-Myc, Cyclin D1, and E2F1 mRNA, while upregulating p21 and leaving p16 unchanged.
    • NaBu treatment significantly increased ROS levels in tumor cells.

    Conclusions:

    • HDAC inhibitors, including NaBu, are potent inducers of cellular senescence in various cancer types.
    • The induction of senescence by HDAC inhibitors involves epigenetic modifications and is associated with increased ROS production.
    • Targeting HDACs represents a viable strategy for cancer treatment by promoting tumor cell senescence and suppression.

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