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Farnesylpyridinium, an analog of isoprenoid farnesol, induces apoptosis but suppresses apoptotic body formation in human promyelocytic leukemia cells
Author(s) -
Hamada Masahiro,
Nishio Kyo-ichi,
Doe Matsumi,
Usuki Yoshinosuke,
Tanaka Toshio
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02373-6
Subject(s) - apoptosis , dna fragmentation , fragmentation (computing) , microbiology and biotechnology , chemistry , cytochrome c , apoptotic dna fragmentation , programmed cell death , biology , biochemistry , ecology
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 c 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.