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NCI CANCERLIT® Search: AIDS-Related Kaposi's Sarcoma - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
Table of Contents
1
UI - 11894131
AU - Mori S; Murakami-Mori K; Nakamura S; Bonavida B
TI -
Actinomycin D-mediated sensitization of AIDS-Kaposi's sarcoma cells to
Fas-mediated apoptosis: involvement of the mitochondrion-dependent
pathway.
SO - Int J Oncol 2002 Apr;20(4):819-26
AD - Department of Microbiology, Immunology, and Molecular Genetics, UCLA
School of Medicine, University of California, Los Angeles, CA 90095,
USA.
Fas engagement rapidly induces formation of the death-inducing signaling
complex (DISC) that consists of Fas, FADD and pro-caspase-8. Activated
caspase-8 at the DISC directly activates downstream caspases, resulting
in induction of apoptosis of the independent mitochondria. In this
study, we have obtained evidence demonstrating that Fas-mediated
apoptosis in AIDS-KS cells takes place in a mitochondria-dependent
manner. FADD and pro-caspase-8 were detected in immunoprecipitates with
anti-Fas antibody in anti-Fas mAb (CH-11)-treated Hut 78, a typical
Fas-sensitive cell line. On the other hand, DISC formation by CH-11 was
markedly reduced in AIDS-KS cells. In addition, CH-11-induced activation
of caspase-8-like protease in AIDS-KS cells was much less pronounced
compared with that in Hut 78; however, a caspase-8 inhibitor, zIETD-fmk,
completely blocked the apoptosis. Further, a caspase-9 inhibitor,
zLEHD-fmk, markedly inhibited Fas-mediated apoptosis in AIDS-KS cells.
Several apoptotic stimuli induce mitochondria activation allowing
cytochrome c release from the mitochondria. In the apoptosome,
cytochrome c and Apaf-1 activate caspase-9 which subsequently leads to
the activation of caspase-3. In AIDS-KS cells, CH-11 triggered
cytochrome c release, an event which was inhibited by zIETD-fmk.
Further, a caspase-3 inhibitor, zDEVD-fmk completely inhibited the
apoptosis. Altogether, the present data provide evidence that the Fas
signal in AIDS-KS cells is preferentially transduced through the
mitochondria-dependent pathway, which is initiated by caspase-8
activation.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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