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Blood, 15 December 2001, Vol. 98, No. 13, pp. 3762-3769
NEOPLASIA
Arsenic trioxide induces apoptosis in human T-cell
leukemia virus type 1- and type 2-infected cells by a
caspase-3-dependent mechanism involving Bcl-2 cleavage
Renaud Mahieux,
Cynthia Pise-Masison,
Antoine Gessain,
John. N. Brady,
René Olivier,
Emmanuelle Perret,
Tom Misteli, and
Christophe Nicot
From Unité d'Epidémiologie et
Physiopathologie des Virus Oncogènes and Unité d'Oncologie
Virale, Institut Pasteur; and the Virus Tumor Biology Section
and the Laboratory of Receptor Biology and Gene Expression, National
Cancer Institute, National Institutes of Health, Bethesda, MD.
Treatment of patients with adult T-cell leukemia-lymphoma (ATLL)
using conventional chemotherapy has limited benefit because human
T-cell leukemia virus type 1 (HTLV-1) cells are resistant to most
apoptosis-inducing agents. The recent report that arsenic trioxide
induces apoptosis in HTLV-1-transformed cells prompted investigation
of the mechanism of action of this drug in HTLV-1 and HTLV-2
interleukin-2-independent T cells and in HTLV-1-immortalized cells or
in ex vivo ATLL samples. Fluorescence-activated cell sorter
analysis, fluorescence microscopy, and measures of mitochondrial membrane potential (  m) demonstrated that arsenic trioxide alone was sufficient to induce programmed cell death in all HTLV-1 and -2 cells tested and in ATLL patient samples. I B- phosphorylation strongly decreased, and NF-B translocation to the nucleus was abrogated. Expression of the antiapoptotic protein
Bcl-XL, whose promoter is NF-B dependent, was
down-regulated. The collapse of m and the release of
cytochrome c to the cytosol resulted in the activation of
caspase-3, as demonstrated by the cleavage of PARP. A specific
caspase-3 inhibitor (Ac-DEVD-CHO) could reverse this phenotype. The
antiapoptotic factor Bcl-2 was then cleaved, converting it to a
Bax-like death effector. These results demonstrated that arsenic
trioxide induces apoptosis in HTLV-1- and -2-infected cells through
activation of the caspase pathway.
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