Cyclovirobuxine D Induces Autophagy-Associated Cell Death via the Akt/mTOR Pathway in MCF-7 Human Breast Cancer Cells
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- Lu Jing
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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- Sun Duanping
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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- Gao Si
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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- Gao Ying
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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- Ye Jiantao
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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- Liu Peiqing
- Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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抄録
Autophagy is a highly regulated and multi-step biological process that serves to remove damaged cytoplasmic components and organelles. It has been suggested that the activation of autophagy may be a promising therapeutic strategy for cancer treatment by triggering cell death. In this study, we reported that cyclovirobuxine D (CVB-D), an alkaloid component in a traditional Chinese herb, could induce autophagy in the MCF-7 human breast cancer cell line. CVB-D inhibited the viability of MCF-7 cells in a concentration- and time-dependent manner. Activation of autophagy was characterized by transmission electron microscopy, monodansylcadaverine staining, and expression of autophagy marker microtubule-associated protein 1 light chain 3 (LC3). After CVB-D treatment, a clear accumulation of autophagosomes was observed accompanied with elevated LC3 fluorescent puncta. Western blot analysis revealed that CVB-D significantly promoted the conversion from LC3-I to LC3-II and the expression of autophagy-related protein 5 (ATG5), which are both essential for autophagosome formation. On the other hand, CVB-D–induced autophagy and decrease in cell viability could be blocked by 3-methyladenine, a well-established autophagy inhibitor. Moreover, CVB-D attenuated the phosphorylation of Akt and mTOR, two pivotal suppressors in autophagy pathways. These findings shed new light on the pharmacological actions and mechanism of CVB-D and may support the potential utility of autophagy inducers in cancer treatment.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 125 (1), 74-82, 2014
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680157032832
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- NII論文ID
- 130003391522
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC2cXptlSisLY%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 025463162
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- PubMed
- 24758922
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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