Potentiation of Bleomycin in Jurkat Cells by Fungal Pycnidione

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  • Kaneko Mayumi
    Graduate School of Pharmaceutical Sciences, Kitasato University
  • Matsuda Daisuke
    Graduate School of Pharmaceutical Sciences, Kitasato University
  • Ohtawa Masaki
    Graduate School of Pharmaceutical Sciences, Kitasato University
  • Fukuda Takashi
    Kitasato Institute for Life Sciences and Graduate School of Infection Control Sciences, Kitasato University
  • Nagamitsu Tohru
    Graduate School of Pharmaceutical Sciences, Kitasato University
  • Yamori Takao
    Division of Molecular Pharmacology, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research
  • Tomoda Hiroshi
    Graduate School of Pharmaceutical Sciences, Kitasato University

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Most cancer cells have mutations in genes at the G1 checkpoint and repair DNA only in the G2 phase; therefore, the G2 checkpoint is a potential target to develop novel therapy. In the course of screening, a known compound, pycnidione, was isolated from the fungal culture broth of Gloeotinia sp. FKI-3416. Pycnidione irreversibly abrogated bleomycin-induced G2 arrest in Jurkat cells and synergically potentiated the cytotoxicity of bleomycin. To elucidate the mechanism of action, the effect of pycnidione on the signal transduction of the G2 checkpoint was analyzed, showing that the increased phospho-cyclin dependent kinase-1 (CDK1) level caused by bleomycin was abrogated in the presence of pycnidione, indicating that cells did not arrest at the G2 phase. Moreover, under these conditions, Chk1 and Chk2 levels were markedly down-regulated. Thus, we concluded that pycnidione abrogated bleomycin-induced G2 arrest by decreasing Chk1 and Chk2.

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