Open AccessDifferential inhibition of radiation‐induced apoptosis
Author(s) -
HaimovitzFriedman Adriana,
Kolesnick Richard N.,
Fuks Zvi
Publication year - 1997
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.5530150708
Subject(s) - biology , ceramide , apoptosis , microbiology and biotechnology , signal transduction , crosstalk , dna damage , lipid signaling , programmed cell death , sphingomyelin , cancer research , dna , biochemistry , enzyme , physics , optics , membrane
The most common mechanism by which radiation kills cells is the induction of DNA double‐strand breaks that results in the loss of cell proliferation. Even though apoptosis is increasingly identified in experimental systems in vitro and in vivo, it is still generally regarded as a rare mode of radiation‐induced cell kill with minor relevance for the clinical effects of radiation. This review will focus on pro‐ and antiapoptotic signaling that affects the apoptotic outcome in irradiated mammalian cells. In particular, we will concentrate on the sphingomyelin/ceramide signal transduction pathway which is involved in initiation of stress‐induced apoptosis in a variety of normal and neoplastic cells. We will also discuss the crosstalk between the sphingomyelin/ceramide pathway and the protein kinase C pathway which constitutes an antiapoptotic pathway, and the potential for pharmacological modulation to increase the fraction of apoptotic cells undergoing apoptosis after radiation exposure. Stem Cells 1997; 15 (suppl 2): 43–47