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Blood, Vol. 95 No. 6 (March 15), 2000:
pp. 2111-2117
Growth of FasL-bearing tumor cells in syngeneic murine host
induces apoptosis and toxicity in Fas+ organs
Ahmet Zeytun,
Mitzi Nagarkatti, and
Prakash S. Nagarkatti
From the Department of Biology and the Department of Biomedical
Sciences and Pathobiology, Virginia-Maryland College of Veterinary
Medicine, Virginia Polytechnic Institute and State University,
Blacksburg, VA.
In the current study, we investigated whether the growth of
FasL-bearing tumor cells would induce apoptosis and toxicity in organs
that express high level of Fas. Sera from C57BL/6 +/+
(wild-type) mice injected with syngeneic FasL+ tumors,
LSA, or EL-4, showed significantly higher levels of soluble FasL than
that from the nontumor-bearing mice. Furthermore, the soluble FasL was
functional inasmuch as the sera from tumor-bearing mice were able to
induce apoptosis in Fas+ but not Fas
targets. Histopathologic studies and in situ TUNEL assay to detect apoptosis were carried out in C57BL/6 +/+
(Fas+) or C57BL/6 lpr/lpr (Fas)
mice injected with syngeneic LSA and EL-4 tumor cells. The morphology of the liver and thymus from tumor bearing C57BL/6 +/+ mice
showed marked damage and tissue destruction. In contrast, the liver and thymus from tumor-bearing C57BL/6 lpr/lpr mice showed minimal damage. Furthermore, the tumor-bearing C57BL/6 +/+, but not the C57BL/6 lpr/lpr, mice exhibited significant apoptosis in the
liver and thymus. The FasL responsible for toxicity was tumor derived rather than host derived; tumor-bearing C57BL/6 gld/gld
(FasL-defective) mice also exhibited significant apoptosis in the liver
and thymus. Together, these data suggested that the in vivo growth of
FasL-bearing tumor cells can induce significant apoptosis and toxicity
in Fas+ tissues of the host. Such toxicity may be
mediated by the soluble FasL produced by tumor cells.
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