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National Institute of Environmental Health Sciences

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Publication Detail

Title: Unsymmetrically substituted polyamine analogue induces caspase-independent programmed cell death in Bcl-2-overexpressing cells.

Authors: Ha, H C; Woster, P M; Casero Jr, R A

Published In Cancer Res, (1998 Jul 1)

Abstract: The polyamine analogue, N1-ethyl-N11-[(cycloheptyl)methyl]-4,8-diazaundecane (CHENSpm)-induced programmed cell death in NCI H157 cells is accompanied by cytochrome c release, the loss of mitochondrial membrane potential, activation of caspase-3, caspase-mediated poly(ADP-ribose) polymerase cleavage, G2-M arrest, and DNA and nuclear fragmentation. Overexpression of Bcl-2 completely inhibits CHENSpm-induced cytochrome c release, caspase-3 activation, and poly(ADP-ribose) polymerase cleavage. However, Bcl-2 does not abrogate CHENSpm-induced programmed cell death. These results suggest that although cytochrome c release and activation of the caspase-3 protease cascade contribute to the rapid and efficient execution of apoptosis, a caspase cascade-independent pathway also exists and can be activated by CHENSpm treatment.

PubMed ID: 9661878 Exiting the NIEHS site

MeSH Terms: Antineoplastic Agents/pharmacology*; Apoptosis/drug effects*; Apoptosis/genetics; Caspases*; Cysteine Endopeptidases/metabolism*; Cytochrome c Group/drug effects; Cytochrome c Group/metabolism; DNA Fragmentation/drug effects; DNA, Neoplasm/drug effects; G2 Phase/drug effects; Humans; Membrane Potentials/drug effects; Mitochondria/drug effects; Mitochondria/metabolism; Mitosis/drug effects; Neoplasm Proteins/metabolism*; Poly(ADP-ribose) Polymerases/metabolism; Polyamines/pharmacology*; Proto-Oncogene Proteins c-bcl-2/metabolism*; Research Support, U.S. Gov't, P.H.S.

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