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Blood, 15 October 2000, Vol. 96, No. 8, pp. 2849-2855
NEOPLASIA
Arsenic-interferon- -triggered apoptosis in HTLV-I transformed
cells is associated with Tax down-regulation and reversal of
NF- B activation
Marwan E. El-Sabban,
Rihab Nasr,
Ghassan Dbaibo,
Olivier Hermine,
Nour Abboushi,
Frédérique Quignon,
Jean Claude Ameisen,
Françoise Bex,
Hugues de
Thé, and
Ali Bazarbachi
From the Departments of Human Morphology, Internal
Medicine, Biochemistry, and Pediatrics, Faculty of Medicine, American
University of Beirut, Beirut, Lebanon; CNRS URA 1461 and Department of
Hematology, Necker Hospital, Paris, France; UPR 9051 CNRS Laboratoire
associé No. 11 du comité de Paris de la Ligue contre le
Cancer, conventionné par l'Université Paris VII,
Hôpital St Louis, Paris, France; INSERM CJF 9701, Hôpital
Bichat, Paris, France; and Departement de Biologie Moléculaire,
Université Libre de Bruxelles, Brussels, Belgium.
Human T-cell lymphotropic virus type I (HTLV-I)-associated
adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature activated T cells resistant to conventional chemotherapy. The viral
transactivator protein Tax plays a critical role in
HTLV-I-induced transformation and apoptosis resistance by inducing
I B- degradation, resulting in the activation of the
NF-Bpathway. In these HTLV-I-transformed cells, arsenic trioxide
(As) and interferon (IFN)- synergize to induce cell cycle arrest and
apoptosis. We demonstrate that cell death induction is only partly
dependent upon caspase activation and is not associated with modulation
of bcl-2, bax, or p53 expression. However, combined As and IFN induce
the degradation of Tax, associated with an up-regulation of IB-
resulting in a sharp decrease in RelA DNA binding nuclear factor
(NF)-B complexes because of the cytoplasmic retention of RelA. Taken
the role of Tax in HTLV-I-induced transformation, its down-regulation
probably accounts for cell death induction through inactivation of the
NF-B pathway. Such specific targeting of the viral oncoprotein by
As-IFN treatment, reminiscent of As targeting of promyelocytic
leukemia/retinoic acid receptor- in acute promyelocytic
leukemia, provides strong rational for combined As-IFN therapy in ATL patients.
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