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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  • Waiwut Pornthip
    Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama
  • Shin Myoung-Sook
    Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama
  • Yokoyama Satoru
    Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama
  • 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

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

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Abstract

Gomisin A, a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra chinensis, 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.

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