beta-hydroxyisovalerylshikonin inhibits the cell growth of various   cancer cell lines and induces apoptosis in leukemia HL-60 cells through   a mechanism different from those of Fas and etoposide

CORC > 北京大学 > 化学与分子工程学院

	beta-hydroxyisovalerylshikonin inhibits the cell growth of various cancer cell lines and induces apoptosis in leukemia HL-60 cells through a mechanism different from those of Fas and etoposide
	Hashimoto, S ; Xu, M ; Masuda, Y ; Aiuchi, T ; Nakajo, S ; Cao, JD ; Miyakoshi, M ; Ida, Y ; Nakaya, K
刊名	生物期刊
	1999
关键词	apoptosis JNK leukemia cells MAP kinase shikonin MEDIATED DNA CLEAVAGE POTENT INDUCER ANTICANCER DRUGS TOPOISOMERASE-I INDUCTION CAMPTOTHECIN ACTIVATION NAPHTHOQUINONES THYMOCYTES CISPLATIN
英文摘要	beta-Hydroxyisovalerylshikonin (beta-HIVS), which was isolated from the plant, Lithospermium radix, inhibited the growth of various lines of cancer cells derived from human solid tumors at low concentrations between 10(-8) and 10(-6) M. When HL-60 cells were treated with 10(-6) M beta-HIVS for 3 h, characteristic features of apoptosis, such as DNA fragmentation, nuclear fragmentation, and activation of caspase-3-like activity, were observed. The most characteristic features of the effect of beta-HIVS were the remarkable morphological changes induced upon treatment of HL-60 cells with beta-HIVS, as visualized on the staining of actin filaments with phalloidin labeled with tetramethylrhodamine B isothiocyanate. Moreover, activation of MAP kinases, such as ERK2, JNK and p38, was detected after treatment with 10(-6) M beta-HIVS preceding the appearance of the characteristics of apoptosis, and the features of the activation of these MAP kinases were quite different from those of Fas and anticancer drug-induced apoptosis. The activation of JNK by beta-HIVS was not inhibited by inhibitors of caspases, suggesting that JNK is located either upstream or independent of the caspase signaling pathway. beta-HIVS did not inhibit the activity of topoisomerase II. These results indicate that beta-HIVS induces apoptosis in HL-60 cells through a mechanism unlike those reported for anti-Fas antibodies and etoposide.; Biochemistry & Molecular Biology; SCI(E); 49; ARTICLE; 1; 17-23; 125
语种	英语
内容类型	期刊论文
源URL	[http://ir.pku.edu.cn/handle/20.500.11897/401591]
专题	化学与分子工程学院
推荐引用方式 GB/T 7714	Hashimoto, S,Xu, M,Masuda, Y,et al. beta-hydroxyisovalerylshikonin inhibits the cell growth of various cancer cell lines and induces apoptosis in leukemia HL-60 cells through a mechanism different from those of Fas and etoposide[J]. 生物期刊,1999.
APA	Hashimoto, S.,Xu, M.,Masuda, Y.,Aiuchi, T.,Nakajo, S.,...&Nakaya, K.(1999).beta-hydroxyisovalerylshikonin inhibits the cell growth of various cancer cell lines and induces apoptosis in leukemia HL-60 cells through a mechanism different from those of Fas and etoposide.生物期刊.
MLA	Hashimoto, S,et al."beta-hydroxyisovalerylshikonin inhibits the cell growth of various cancer cell lines and induces apoptosis in leukemia HL-60 cells through a mechanism different from those of Fas and etoposide".生物期刊 (1999).