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    題名: NF-B pathway is involved in griseofulvin-induced G2/M arrest and apoptosis in HL60 cells
    作者: 何元順
    Yih-Huei Uen;Der-Zen Liu;Meng-Shih Weng;Yuan-Soon Ho;Shyr-Yi Lin
    貢獻者: 醫學檢驗暨生物技術學系
    關鍵詞: Law enforcement arrest;Not free of;Apoptosis;M cell
    日期: 2007
    上傳時間: 2009-08-25 10:38:45 (UTC+8)
    摘要: Griseofulvin (GF), an oral antifungal agent, has been shown to exert antitumorigenesis effect through
    G2/Mcell cycle arrest in colon cancer cells. But the underlying mechanisms remained obscure. The purpose of this study is
    to test the cytotoxic effect of GF on HL-60 and HT-29 cells and elucidate its underlying molecular pathways. Dosedependent
    and time-course studies byflowcytometry demonstrated that 30 to 60 mMGF significantly inducedG2/M arrest
    and to a less extend, apoptosis, in HL-60 cells. In contrast, only G2/M arrest was observed in HT-29 cells under similar
    condition. Pretreatment of 30 mM TPCK, a serine protease inhibitor, completely reversed GF-induced G2/M cell cycle
    arrest and apoptosis in HL-60 cells but not in HT-29 cells. The GF-induced G2/M arrest in HL-60 cells is reversible. Using
    EMSA and super-shift analysis, we demonstrated that GF stimulated NF-kB binding activity in HL-60 cells, which was
    completely inhibited by pretreatment of TPCK. Treatment of HL-60 with 30 mMGF activated JNK but not ERK or p38MAPK
    and subsequently resulted in phosporylation of Bcl-2. Pretreatment of TPCK to HL-60 cells blocked the GF-induced Bcl-2
    phosphorylation but not JNK activation. Time course study demonstrated that activation of cdc-2 kinase activity by GF
    correlated with Bcl-2 phosphorylation. Taken together, our results suggest that activation of NF-kB pathway with cdc-2
    activation and phosphorylation of Bcl-2 might be involved in G2/M cell cycle arrest in HL-60 cells. J. Cell. Biochem. 101:
    1165–1175, 2007.
    關聯: J. Cellular Biochemistry.(101):1165-1175.
    資料類型: article
    顯示於類別:[醫學檢驗暨生物技術學系所] 期刊論文

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