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J Biol Chem, Vol. 275, Issue 15, 11154-11163, April 14, 2000
From the The transactivator protein Tax of human T-cell
leukemia virus type I plays an important role in the development of
adult T-cell leukemia probably through modulation of growth regulatory
molecules including p16INK4a. The molecular mechanism
of leukemogenesis induced by Tax has yet to be elucidated. We analyzed
Tax function in the cell cycle using an interleukin-2
(IL-2)-dependent human T-cell line (Kit 225) that can
undergo cell cycle arrest at G0/G1 phase by
deprivation of IL-2. Tax activated endogenous E2F activity in
IL-2-starved Kit 225 cells, resulting in activation of E2F
site-carrying promoters of genes involved in G1 to S phase
transition in a cell type-dependent and
p16INK4a-independent manner. The ability of Tax mutants to
activate E2F coincided with that to activate nuclear factors
Cell Type-specific E2F Activation and Cell Cycle Progression
Induced by the Oncogene Product Tax of Human T-cell Leukemia Virus Type
I*
,,,, and¶
Human Gene Sciences Center and the
§ Department of Microbiology, School of Medicine, Tokyo
Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku,
Tokyo 113-8510, Japan
B and
AT, sole expression of which, however, did not activate E2F, suggesting involvement of another pathway in activation of E2F. Introduction of
Tax by a recombinant adenovirus induced cell cycle progression to
G2/M phase in resting Kit 225 cells accompanied by
endogenous cyclin D2 gene expression. Similarly, Tax-induced cell cycle
progression was seen with peripheral blood lymphocytes prestimulated
with phytohemagglutinin. Analyses with Tax mutants did not allow
Tax-induced cell cycle progression to be differentiated from
Tax-dependent activation of E2F, suggesting that Tax
induces cell cycle progression presumably through activation of E2F.
Nevertheless, infection with an E2F1-expressing virus, which is
sufficient for induction of S phase in serum-starved fibroblasts, was
not sufficient for either E2F activation or cell cycle progression in
IL-2-starved Kit 225 cells, implying differential regulation of E2F
activation and cell cycle progression in T-cells that is activated by Tax.
*
This work was supported in part by a grant-in-aid for
general scientific research and cancer research from the Ministry of Education, Science, Sports and Culture; by a grant from the Core Research for Evolutional Science and Technology (CREST) of the Japan
Science and Technology Corp.; by a grant from the NOVARTIS Foundation
for the Promotion of Science (Japan); and by a grant from the Osaka
Cancer Foundation.The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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