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Blood, 15 August 2001, Vol. 98, No. 4, pp. 1200-1208
NEOPLASIA
The contribution of NF- B activity to spontaneous proliferation
and resistance to apoptosis in human T-cell leukemia virus type 1 Tax-induced tumors
Toni Portis,
John C. Harding, and
Lee Ratner
From the Departments of Medicine, Pathology, and
Molecular Microbiology, Washington University School of Medicine, St
Louis, MO.
Human T-cell leukemia virus type I is the etiologic agent of adult
T-cell leukemia/lymphoma. The Tax protein of this virus is thought to
contribute to cellular transformation and tumor development. In this
report, we have used a Tax transgenic mouse model of tumorigenesis to
study the contribution of nuclear factor (NF)- B activity to
spontaneous tumor cell proliferation and resistance to apoptosis. We
have demonstrated elevated expression levels of NF-B-inducible
cytokines, including interleukin (IL)-6, IL-10, IL-15, and interferon
(IFN)- , in freshly isolated primary tumors from Tax transgenic mice.
Inhibitors of NF-B activity, sodium salicylate and cyclopentenone
prostaglandins (prostaglandin A1 and
15-deoxy- (12,14)-prostaglandin J2), blocked spontaneous
proliferation of Tax transgenic mouse spleen cells. In addition,
Tax-induced tumor cells, which are resistant to irradiation-induced
apoptosis, became sensitive to apoptosis in the presence of sodium
salicylate and prostaglandins. These results strongly suggest that
Tax-mediated induction of NF-B activity contributes to tumorigenesis
in vivo.
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