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Prepublished online as a Blood First Edition Paper on May 13, 2002; DOI 10.1182/blood-2002-01-0151.
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Blood, 1 September 2002, Vol. 100, No. 5, pp. 1828-1834
NEOPLASIA
Bay 11-7082 inhibits transcription factor NF- B and induces
apoptosis of HTLV-I-infected T-cell lines and primary adult T-cell
leukemia cells
Naoki Mori,
Yasuaki Yamada,
Shuichi Ikeda,
Yoshihiro Yamasaki,
Kunihiro Tsukasaki,
Yuetsu Tanaka,
Masao Tomonaga,
Naoki Yamamoto, and
Masahiro Fujii
From the Department of Preventive Medicine and AIDS
Research, Institute of Tropical Medicine, Nagasaki University, Japan;
the Department of Hematology, Molecular Medicine Unit, Atomic Bomb
Disease Institute, and the Department of Laboratory Medicine, Nagasaki
University School of Medicine, Japan; the Department of Internal
Medicine, Sasebo City General Hospital, Japan; the Department of
Internal Medicine, Kokura Memorial Hospital, Kitakyushu, Japan; the
Department of Infectious Disease and Immunology, Okinawa-Asia Research
Center of Medical Science, Faculty of Medicine, University of the
Ryukyus, Nishihara, Okinawa, Japan; and the Division of Virology,
Niigata University Graduate School of Medicine and Dental Sciences,
Japan.
Human T-cell leukemia virus type I (HTLV-I) is the causative agent
of an aggressive form of leukemia designated adult T-cell leukemia
(ATL). We have previously demonstrated that all T-cell lines infected
with HTLV-I and primary leukemic cells from ATL patients display
constitutively high activity of transcription factor NF- B. In this
study we showed that Bay 11-7082, an inhibitor of NF-B, induced
apoptosis of HTLV-I-infected T-cell lines but only negligible
apoptosis of HTLV-I-negative T cells. Bay 11-7082 rapidly and
efficiently reduced the DNA binding of NF-B in HTLV-I-infected T-cell lines and down-regulated the expression of the antiapoptotic gene, Bcl-xL, regulated by NF-B, whereas it had little
effect on the DNA binding of another transcription factor, AP-1.
Although the viral protein Tax is an activator of NF-B, Bay
11-7082-induced apoptosis of HTLV-I-infected cells was not associated
with reduced expression of Tax. Furthermore, Bay 11-7082- induced
apoptosis of primary ATL cells was more prominent than that of normal
peripheral blood mononuclear cells, and apoptosis of these cells was
also associated with down-regulation of NF-B activity. Our results indicate that NF-B plays a crucial role in the pathogenesis and survival of HTLV-I-infected leukemic cells and that it is a suitable target for the prevention and treatment of ATL.
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