Isoegomaketone Induces Apoptosis through Caspase-Dependent and Caspase-Independent Pathways in Human DLD1 Cells
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- CHO Byoung Ok
- Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute
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- JIN Chang Hyun
- Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute
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- PARK Yong Dae
- Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute
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- RYU Hyung Won
- Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute
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- BYUN Myung Woo
- Department of Culinary Nutrition, Woosong University
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- SEO Kwon Il
- Department of Food and Nutrition, Sunchon National University
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- JEONG Il Yun
- Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute
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抄録
Isoegomaketone (IK) is an essential oil component of Perilla frutescens (L.), but the mechanism by which IK induces apoptosis has never been studied. The purpose of this study was to elucidate the IK-induced apoptotic pathway in DLD1 human colon cancer cells. We observed that IK treatment over 24 h significantly inhibited cell viability in a dose-dependent manner. We also found that IK triggered cleavage of PARP. Moreover, IK treatment resulted in cleavage of caspase-8, -9, and -3 in a dose- and time-dependent manner. IK treatment also resulted in cleavage of Bid and translocation of Bax, and triggered the release of cytochrome c from the mitochondria to the cytoplasm. Furthermore, it resulted in the translocation of apoptosis inducing factor (AIF), a caspase-independent mitochondrial apoptosis factor, from the mitochondria into the nucleus. Overall, these results suggest that IK induces apoptosis through caspase-dependent and capase-independent pathways in DLD1 cells.
収録刊行物
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- Bioscience, Biotechnology, and Biochemistry
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Bioscience, Biotechnology, and Biochemistry 75 (7), 1306-1311, 2011
公益社団法人 日本農芸化学会
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詳細情報 詳細情報について
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- CRID
- 1390282681453660544
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- NII論文ID
- 10029329187
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- NII書誌ID
- AA10824164
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- ISSN
- 13476947
- 09168451
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- NDL書誌ID
- 11174286
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- PubMed
- 21737934
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可