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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 275-281
Bcl-XL is up-regulated by HTLV-I and HTLV-II in vitro
and in ex vivo ATLL samples
Christophe Nicot,
Renaud Mahieux,
Shigeki Takemoto, and
Genoveffa Franchini
From the Basic Research Laboratory Division of Basic Sciences,
Laboratory of Receptor Biology and Gene Expression, National
Cancer Institute, National Institutes of Health, Bethesda, MD.
Human T lymphotropic virus type I (HTLV-I) is the etiological agent
of adult T-cell lymphocytic leukemia (ATLL), whereas HTLV-II has not
been associated with hematopoietic malignancies. The control of
apoptotic pathways has emerged as a critical step in the development of
many cancer types. As a result, the underlying mechanism of long-term
survival of HTLV-I and HTLV-II was studied in infected T cells in vitro
and in ex vivo ATLL samples. Results indicate that HTLV-I- and
HTLV-II-infected T cells in vitro express high levels of the
antiapoptotic protein Bcl compared with other human leukemic T cell lines or uninfected peripheral blood mononuclear cells.
The levels of proapoptotic proteins Bax, BAD, and Bak were not
significantly altered. HTLV-I and HTLV-II viral transactivators, Tax1
and Tax2, are known to increase expression of cellular genes. These
proteins were tested for increased transcription from the human Bcl2
and Bcl-XL promoters. Whereas no effect was observed on the
Bcl2 promoter, both Tax1 and Tax2 increased transcription of the
Bcl-XL promoter in T cells, although Tax1 appeared to be more efficient than Tax2. The biological significance of these observations was validated by the finding of an increased expression of
Bcl-XL in ex vivo ATLL cells, especially from patients
unresponsive to various chemotherapy regimens. Altogether, these data
suggest that overexpression of Bcl-XL in vivo
may be in part responsible for the resistance of ATLL cells to
chemotherapy. In addition, inefficient activation of the
Bcl-XL promoter by Tax2 may result in a shorter survival
time of HTLV-II-infected cells in vivo and a diminished risk of
leukemia development.
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