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Blood, Vol. 95 No. 12 (June 15), 2000:
pp. 3915-3921
Constitutive activation of transcription factor AP-1 in primary
adult T-cell leukemia cells
Naoki Mori,
Masahiro Fujii,
Kousuke Iwai,
Shuichi Ikeda,
Yoshihiro Yamasaki,
Tomoko Hata,
Yasuaki Yamada,
Yuetsu Tanaka,
Masao Tomonaga, and
Naoki Yamamoto
From the Department of Preventive Medicine and AIDS Research,
Institute of Tropical Medicine, Nagasaki University, Nagasaki, Japan;
Department of Laboratory Medicine, Nagasaki University School of
Medicine, Nagasaki, Japan; Department of Hematology, Atomic Disease
Institute, Nagasaki University School of Medicine, Nagasaki, Japan;
Department of Internal Medicine, City of Sasebo General Hospital,
Sasebo, Japan; Department of Internal Medicine, Kokura Memorial
Hospital, Kitakyushu, Japan; Department of Infectious Disease and
Immunology, Okinawa-Asia Research Center of Medical Science, Faculty of
Medicine, University of the Ryukyus, Okinawa, Japan; Department of
Virology, Niigata University School of Medicine, Niigata, Japan.
Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent
of adult T-cell leukemia (ATL). This study examined the status of the
oncogenic transcription factor AP-1 in leukemic cells freshly isolated
from patients with ATL. Leukemic cells from peripheral blood of all
patients with ATL exhibited constitutive AP-1 DNA binding activity,
whereas mononuclear cells from normal individuals did not. In agreement
with previous studies, HTLV-I transforming protein, Tax, was found to
stimulate the DNA binding activity of AP-1 in a T-cell line. However,
HTLV-I genes, including Tax, were not significantly expressed in
leukemic cells freshly obtained from patients with ATL. Moreover, all
T-cell lines derived from leukemic cells of patients with ATL also
displayed constitutive AP-1 DNA binding activity, but expressed little
Tax protein. Thus, leukemic cells of patients with ATL appear to have
Tax-independent mechanisms that induce AP-1 activity, both in vivo and
in vitro. In antibody supershift experiments, AP-1 in fresh leukemic
cells and ATL-derived cell lines were found to contain JunD.
Consistently, all primary ATL cells and ATL-derived cell lines
expressed high levels of JunD messenger RNA. Our results suggest that
AP-1 is activated in leukemic cells of patients with ATL through a
Tax-independent mechanism and this may play a role in the deregulated
phenotypes of ATL leukemic cells.
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