Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways.

CMUR > College of Life Sciences > Department of Biological Science and Technology > Journal articles > Item 310903500/6290

Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/6290

Title:	Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways.
Authors:	(Shuw-Yuan Lin)、(Wan-Wen Lai)、(Chin-Chin Ho)、游富順、(Guang-Wei Chen)、楊家欣(Yang Jai-Sing)、(Kuo-Ching Liu)、林孟亮(Meng-Liang Lin)、吳玢玢、(Ming-Jen Fan)、鍾景光(Jing-Gung Chung)*
Contributors:	生命科學院生物科技學系;中國附醫醫學研究部
Keywords:	ROS;ER stress;cell death;anthraquinone
Date:	2009.03
Issue Date:	2009-08-25 14:39:54 (UTC+8)
Abstract:	Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment of human tongue cancer SCC-4 cells with various concentrations of emodin led to G2/M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (ΔΨm) and a decrease in the ratio of mitochondrial Bcl-2 and Bax content; emodin also promoted the levels of GADD153 and GRP78. The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together, these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Bax modulation, mitochondrial cytochrome c release and caspase activation, consequently leading to apoptosis in SCC-4 cells.
Relation:	ANTICANCER RESEARCH 29( )327 ~336
Appears in Collections:	[Department of Biological Science and Technology] Journal articles

Files in This Item:

File	Size	Format
	0Kb	Unknown	358	View/Open

Loading...