Farnesylpyridinium, an analog of isoprenoid farnesol, induces apoptosis but suppresses apoptotic body formation in human promyelocytic leukemia cells

被引:8
作者
Hamada, M
Nishio, K
Doe, M
Usuki, Y
Tanaka, T
机构
[1] Osaka City Univ, Grad Sch Sci, Dept Bio & Geosci, Sumiyoshi Ku, Osaka 5588585, Japan
[2] Osaka City Univ, Grad Sch Sci, Div Mol Mat Sci, Sumiyoshi Ku, Osaka 5588585, Japan
来源
FEBS LETTERS | 2002年 / 514卷 / 2-3期
关键词
apoptosis; HL-60; cells; farnesol; apoptotic body; actin;
D O I
10.1016/S0014-5793(02)02373-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
1-Farnesylpyridinium (FPy), an analog of isoprenoid farnesol, initially induced morphological changes similar to those of typical apoptosis in human leukemia HL-60 cells but FPy-treated cells were characterized by the absolute absence of final apoptotic events such as fragmentation into apoptotic bodies. FPy-induced cell death was considered to be apoptotic on the basis of the induction of DNA fragmentation and the protection against these events by the coaddition of a pan-caspase inhibitor. The increase in the cytoplasmic cytochrome e level supported the possibility that FPy-treated cells should have the ability to complete the entire apoptotic process ending in cell fragmentation and apoptotic body formation. At concentrations too low to induce apoptosis, FPy could suppress the induction of apoptotic body formation in HL-60 cells by typical inducers of apoptosis such as actinomycin D or anisomycin. FPy exhibited a cytochalasin-like effect on spatial arrangement of actin filament independent of its apoptosis-inducing activity. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:250 / 254
页数:5
相关论文
共 36 条
[1]   DIFFERENCES IN SENSITIVITY TO FARNESOL TOXICITY BETWEEN NEOPLASTICALLY-DERIVED AND NON-NEOPLASTICALLY-DERIVED CELLS IN CULTURE [J].
ADANY, I ;
YAZLOVITSKAYA, EM ;
HAUG, JS ;
VOZIYAN, PA ;
MELNYKOVYCH, G .
CANCER LETTERS, 1994, 79 (02) :175-179
[2]   Mechanism of dibucaine-induced apoptosis in promyelocytic leukemia cells (HL-60) [J].
Arita, K ;
Utsumi, T ;
Kato, A ;
Kanno, T ;
Kobuchi, H ;
Inoue, B ;
Akiyama, J ;
Utsumi, K .
BIOCHEMICAL PHARMACOLOGY, 2000, 60 (07) :905-915
[3]  
CHAKRABARTI R, 1991, J BIOL CHEM, V266, P12216
[4]   EFFECTS OF CYTOCHALASIN AND PHALLOIDIN ON ACTIN [J].
COOPER, JA .
JOURNAL OF CELL BIOLOGY, 1987, 105 (04) :1473-1478
[5]  
CORRELL CC, 1994, J BIOL CHEM, V269, P17390
[6]  
COTTER TG, 1992, CANCER RES, V52, P997
[7]  
Egozi Y, 1999, INT J CANCER, V80, P911, DOI 10.1002/(SICI)1097-0215(19990315)80:6<911::AID-IJC18>3.3.CO
[8]  
2-W
[9]   A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD [J].
Enari, M ;
Sakahira, H ;
Yokoyama, H ;
Okawa, K ;
Iwamatsu, A ;
Nagata, S .
NATURE, 1998, 391 (6662) :43-50
[10]   REGULATION OF THE MEVALONATE PATHWAY [J].
GOLDSTEIN, JL ;
BROWN, MS .
NATURE, 1990, 343 (6257) :425-430