Details

Autor(en) / Beteiligte

• Waiwut, Pornthip
• Shin, Myoung-Sook
• Yokoyama, Satoru
• Saiki, Ikuo
• Sakurai, Hiroaki

Titel

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

Ist Teil von

• Biological & pharmaceutical bulletin, 2012-11, Vol.35 (11), p.1997-2003

Ort / Verlag

Tokyo: Japan Science and Technology Agency

Erscheinungsjahr

2012

Link zum Volltext

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• 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.