Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway
文献类型：期刊论文
| 作者 | Huang, Zhiwei; Chen, Guichen; Shi, Ping |
| 刊名 | archives of pharmacal research
 |
| 出版日期 | 2008-06-01 |
| 卷号 | 31期号:6页码:742-748 |
| 关键词 | emodin human breast cancer BCap-37 cells apoptosis the mitochondrial signaling pathway |
| 合作状况 | 其它 |
| 中文摘要 | emodin, a natural anthraquinone compound isolated from the rhizome of rhubarb, is reported to suppress the growth of tumor in many clinical situations. in this study, we focused on the effect of emodin in human breast cancer bcap-37 cells and further understand the underlying molecular mechanism in treating breast cancer. using mtt assay and flow cytometry, we demonstrated the critical role of emodin in the suppression of the proliferation of bcap-37 cells based on a concentration- and time-dependent manner. the increase of apoptotic rate was also observed after incubation of bcap-37 cells on emodin at 20 mu m and 50 mu m for 48 h. the cells exhibited typical apoptotic features including cellular morphological change, chromatin condensation and membrane blebbing. the results of the study further showed that bcl-2 level decreased, while bax and cytosolic cytochrome c levels in sample cells increased after the emodin treatment by using western blot. the decline in the bcl-2/bax ratio and the increase of cytosolic cytochrome c concentration were consistent with the increase of the apoptotic ratio. the results strongly suggest that the disruption of the mitochondrial signaling pathway was involved in emodin-induced apoptosis in bcap-37 cells. |
| 英文摘要 | emodin, a natural anthraquinone compound isolated from the rhizome of rhubarb, is reported to suppress the growth of tumor in many clinical situations. in this study, we focused on the effect of emodin in human breast cancer bcap-37 cells and further understand the underlying molecular mechanism in treating breast cancer. using mtt assay and flow cytometry, we demonstrated the critical role of emodin in the suppression of the proliferation of bcap-37 cells based on a concentration- and time-dependent manner. the increase of apoptotic rate was also observed after incubation of bcap-37 cells on emodin at 20 mu m and 50 mu m for 48 h. the cells exhibited typical apoptotic features including cellular morphological change, chromatin condensation and membrane blebbing. the results of the study further showed that bcl-2 level decreased, while bax and cytosolic cytochrome c levels in sample cells increased after the emodin treatment by using western blot. the decline in the bcl-2/bax ratio and the increase of cytosolic cytochrome c concentration were consistent with the increase of the apoptotic ratio. the results strongly suggest that the disruption of the mitochondrial signaling pathway was involved in emodin-induced apoptosis in bcap-37 cells. |
| 学科主题 | 药学 |
| WOS标题词 | science & technology ; life sciences & biomedicine |
| 类目[WOS] | chemistry, medicinal ; pharmacology & pharmacy |
| 研究领域[WOS] | pharmacology & pharmacy |
| 关键词[WOS] | gastric-cancer ; hl-60 cells ; growth ; death ; anthraquinones ; cytotoxicity ; mechanisms ; inhibition ; caspases ; survival |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000256838800010 |
| 公开日期 | 2009-12-04 |
| 源URL | [http://ir.nwipb.ac.cn/handle/363003/1209]  |
| 专题 | 西北高原生物研究所_中国科学院西北高原生物研究所 |
| 作者单位 | Chinese Acad Sci, NW Inst Plateau Biol, Xining 810008, Peoples R China |
| 推荐引用方式 GB/T 7714 | Huang, Zhiwei,Chen, Guichen,Shi, Ping. Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway[J]. archives of pharmacal research,2008,31(6):742-748. |
| APA | Huang, Zhiwei,Chen, Guichen,&Shi, Ping.(2008).Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway.archives of pharmacal research,31(6),742-748. |
| MLA | Huang, Zhiwei,et al."Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway".archives of pharmacal research 31.6(2008):742-748. |
入库方式： OAI收割
来源：西北高原生物研究所
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