Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway

	Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway
	Huang, Zhiwei ; Chen, Guichen ; Shi, Ping
刊名	ARCHIVES OF PHARMACAL RESEARCH ; Huang Zhiwei,Chen Guichen,Shi Ping.Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway. ARCHIVES OF PHARMACAL RESEARCH,2008,31(6):742-748
	2008-06-01
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.; 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.
内容类型	期刊论文
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
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, Huang Zhiwei,Chen Guichen,Shi Ping.Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway. ARCHIVES OF PHARMACAL RESEARCH,2008,31(6):742-748,2008.
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.
MLA	Huang, Zhiwei,et al."Emodin-induced apoptosis in human breast cancer BCap-37 cells through the mitochondrial signaling pathway".ARCHIVES OF PHARMACAL RESEARCH (2008).