Coumarin Induces Cell Cycle Arrest and Apoptosis in Human Cervical Cancer HeLa Cells through a Mitochondria- and Caspase-3 Dependent Mechanism and NF-κB Down-regulation

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 醫學檢驗生物技術學系暨碩士班 > 期刊論文 > Item 310903500/1718

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题名:	Coumarin Induces Cell Cycle Arrest and Apoptosis in Human Cervical Cancer HeLa Cells through a Mitochondria- and Caspase-3 Dependent Mechanism and NF-κB Down-regulation
作者:	莊淨媛;黃永豐(Huang Yung-Feng);(Lu Hsu-Feng);何恆堅(Heng-Chien Ho);楊家欣(Yang Jai-Sing);(Li Te-Mao);張乃文(Chang,Nai-Wen);鍾景光(Jing-gung Chung)*
贡献者:	健康照護學院醫學檢驗生物技術學系
关键词:	Coumarin;apoptosis;cell cycle;caspase-3;NF-κB;mitochondria
日期:	2007-03
上传时间:	2009-08-19 17:06:53 (UTC+8)
摘要:	The effects of coumarin on cell viability, cell cycle arrest and induction of apoptosis were investigated in human cervical cancer HeLa cells. Coumarin was cytotoxic with an IC50 of 54.2 μM, induced morphological changes, and caused G0/G1 arrest and apoptosis. The decreasing number of viable cells appeared to be due to induction of cell cycle arrest and apoptotic cell death, since coumarin induced morphologically apoptotic changes and internucleosomal DNA laddering fragmentation and increased the sub-G1 group. Coumarin affected the production of reactive oxygen species and Ca2+ concentration, and dose-dependently induced the depolarization of mitochondrial membrane potential. Also, coumarin treatment gradually decreased the expression of G0/G1-associated proteins which may have led to the G0/G1 arrest, and the anti-apoptotic proteins Bcl-2 and Bcl-xL, and increased the expression of the pro-apoptotic protein Bax. Coumarin decreased the mitochondrial membrane potential and promoted the release of cytochrome c and the activation of caspase-3 before leading to apoptosis. These results provide information on the mechanisms by which coumarin induces cell cycle arrest and apoptosis in human cervical cancer cells (HeLa).
關聯:	IN VIVO 21(6):1003~1010
显示于类别:	[醫學檢驗生物技術學系暨碩士班 ] 期刊論文

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