Gomisin A Enhances Tumor Necrosis Factor-α-Induced G1 Cell Cycle Arrest <i>via</i> Signal Transducer and Activator of Transcription 1-Mediated Phosphorylation of Retinoblastoma Protein

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Author(s)

    • Saiki Ikuo
    • Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama
    • Sakurai Hiroaki
    • Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama|Department of Cancer Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama

Abstract

Gomisin A, a dibenzocyclooctadiene lignan isolated from the fruit of <i>Schisandra chinensis</i>, has been reported as an anti-cancer substance. In this study, we investigated the effects of gomisin A on cancer cell proliferation and cell cycle arrest in HeLa cells. Gomisin A significantly inhibited cell proliferation in a dose-dependent manner after 72 h treatment, especially in the presence of tumor necrosis factor-α (TNF-α), due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation. In addition, gomisin A in combination with TNF-α strongly suppressed the expression of signal transducer and activator of transcription 1 (STAT1). Inhibition of STAT1 pathways by a small-interfering RNA against STAT1 and AG490 Janus kinase (JAK) kinase inhibitor AG490 reduced the cyclin D1 expression and RB phosphorylation, indicating that JAK-mediated STAT1 activation is involved in gomisin A-induced G1 cell cycle arrest.

Journal

  • Biological and Pharmaceutical Bulletin

    Biological and Pharmaceutical Bulletin 35(11), 1997-2003, 2012

    The Pharmaceutical Society of Japan

Codes

  • NII Article ID (NAID)
    130001872260
  • NII NACSIS-CAT ID (NCID)
    AA10885497
  • Text Lang
    ENG
  • ISSN
    0918-6158
  • NDL Article ID
    024032964
  • NDL Call No.
    Z53-V41
  • Data Source
    NDL  J-STAGE 
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