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Blood, 15 February 2002, Vol. 99, No. 4, pp. 1341-1349
NEOPLASIA
Human T-cell leukemia virus type I Tax transactivates the matrix
metalloproteinase-9 gene: potential role in mediating adult T-cell
leukemia invasiveness
Naoki Mori,
Hiroshi Sato,
Toshihisa Hayashibara,
Masachika Senba,
Tomayoshi Hayashi,
Yasuaki Yamada,
Shimeru Kamihira,
Shuichi Ikeda,
Yoshihiro Yamasaki,
Shigeru Morikawa,
Masao Tomonaga,
Romas Geleziunas, and
Naoki Yamamoto
From the Departments of Preventive Medicine and AIDS
Research, and Pathology, Institute of Tropical Medicine, Nagasaki
University, Nagasaki, Japan; the Departments of Biochemistry and
Laboratory Medicine, and the Department of Hematology, Molecular
Medicine Unit, Atomic Disease Institute, Nagasaki University School of
Medicine, Nagasaki, Japan; the Department of Internal Medicine, Sasebo
City General Hospital, Sasebo, Japan; the Department of Internal
Medicine, Kokura Memorial Hospital, Kitakyushu, Japan; the Department
of Pathology First Unit, Shimane Medical University, Izumo, Japan; the
Department of Molecular Virology and Oncology, Cancer Research
Institute, Kanazawa University, Kanazawa, Japan; and Dupont
Pharmaceuticals Company, Wilmington, DE.
Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent
of adult T-cell leukemia (ATL) and of tropical spastic paraparesis/HTLV-I-associated myelopathy. Infiltration of various tissues by circulating leukemic cells is a characteristic of ATL. Matrix metalloproteinases (MMPs), which mediate the degradation of the
basement membrane and extracellular matrix, play an important role in
metastasis and tumor cell dissemination. The aim of this study was to
explore whether expression of MMP-2 and MMP-9 was deregulated by HTLV-I
infection. The data showed that HTLV-I-infected T-cell lines expressed
high levels of MMP-9 compared with uninfected T-cell lines. In
contrast, the levels of the related MMP-2 were not significantly
altered by HTLV-I infection. In addition, the elevated expression of
MMP-9 in HTLV-I-infected cells was attributable to the action of the
viral transactivator protein Tax. The results show that Tax can
activate the MMP-9 promoter and induce MMP-9 expression in T cells,
indicating that the constitutive expression of MMP-9 in virus-infected
cell lines is at least in part mediated by Tax. Activation of the MMP-9
promoter by Tax occurs mainly through the action of NF- B and SP-1.
The biologic significance of these observations was validated by the
following 2 findings: MMP-9 expression was increased in primary ATL
cells, and plasma MMP-9 levels were elevated in ATL patients. In
addition, plasma levels of MMP-9 correlated with organ involvement in
ATL patients. Together these data suggest that overexpression of MMP-9
in HTLV-I- infected cells may be in part responsible for the
invasiveness of ATL cells.
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