Autophagy preceded apoptosis in oridonin-treated human breast cancer MCF- cells
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- Cui Qiao
- China–Japan Research Institute of Medical Pharmaceutical Sciences, Shenyang Pharmaceutical University
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- Tashiro Shin-ichi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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- Onodera Satoshi
- Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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- Minami Mutsuhiko
- Department of Immunology, Yokohama City University School of Medicine
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- Ikejima Takashi
- China–Japan Research Institute of Medical Pharmaceutical Sciences, Shenyang Pharmaceutical University
書誌事項
- タイトル別名
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- Autophagy Preceded Apoptosis in Oridonin-Treated Human Breast Cancer MCF-7 Cells
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説明
Recent studies have shown that MCF-7 cells undergo autophagy under some conditions, such as tamoxifen treatment and starvation. In this study, we investigated autophagy in MCF-7 cells under oridonin treatment and further examined the relationship between autophagy and apoptosis. After 3-MA (the specific inhibitor of autophagy) pre-culture, MCF-7 cells were exposed to oridonin, and the growth inhibitory ratio, morphologic changes, DNA fragmentation, proteins expression, autophagic ratio and apoptotic ratio were evaluated. Oridonin inhibited the proliferation of MCF-7 cells and induced autophagy in vitro. MDC (a specific dye for autophagosome) recruitment and typical apoptotic features, including apoptotic bodies, membrane blebbing as well as nuclear condensation, were induced by oridonin. Oridonin downregulated the phosphorylation of ERK, whereas those of JNK and P38 kinase were upregulated. In the condition of oridonin treatment, 3-MA significantly reduced the autophagic level, and the apoptotic cell ratio was also declined. Furthermore, combined treatment with oridonin and 3-MA upregulated ERK phosphorylation and downregulated JNK and P38 kinases phosphorylation compared with oridonin alone treatment groups, indicating that autophagy facilitated apoptosis in oridonin-induced MCF-7 cells. In addition, 3-MA application downregulated DNA ladder and Bax expression but upregulated Bcl-2 expression, compared with oridonin alone treatment. Taken together, oridonin simultaneously induced MCF-7 cells both apoptosis and autophagy, and in this settings, inhibition of autophagy induced lowered apoptotic level, therefore, autophagy participated in upregulation of apoptosis.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 30 (5), 859-864, 2007
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204627054720
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- NII論文ID
- 110006273281
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 8714132
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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
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