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Prepublished online as a Blood First Edition Paper on January 30, 2003; DOI 10.1182/blood-2002-09-2986.
Submitted October 1, 2002
Accepted January 24, 2003
Arsenic/Interferon specifically reverses two distinct gene networks critical for the survival of HTLV-I infected leukemic cells
Rihab Nasr, Andreas Rosenwald, Marwan E El-Sabban, Bertrand Arnulf, Pierre Zalloua, Yves Lepelletier, Francoise Bex, Olivier Hermine, Louis Staudt, Hugues de The, and Ali Bazarbachi*
Department of Internal Medicine, American University of Beirut, Beirut, Lebanon
Department of Biochemistry, American University of Beirut, Beirut, Lebanon
Department of Human Morphology, American University of Beirut, Beirut, Lebanon
Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
CNRS URA 1461 and Department of Hematology, Necker Hospital, Paris, France
Chronic Care Center, Beirut, Lebanon
Departement de Biologie Moleculaire, Universite Libre de Bruxelles, Brussels, Belgium
UPR 9051, CNRS, Paris, France
* Corresponding author; email: bazarbac{at}aub.edu.lb.
Adult T-cell leukemia (ATL) is a severe chemotherapy-resistant malignancy associated with prolonged infection by the HTLV-I retrovirus. Although the Tax viral transactivator is clearly an oncogene, the role of its continuous expression in the maintenance of the transformed phenotype is controversial. Since arsenic trioxide (As) and interferon alpha (IFN) synergize to induce cell cycle arrest and apoptosis of ATL cells both ex vivo and in vitro, we investigated the effects of As alone and As/IFN combination on gene networks in HTLV-I infected leukemic cells. Arsenic/IFN combination reduced Tax expression and, accordingly, reversed the Tax-induced constitutive NF- B activation. Using DNA microarray analyses, we demonstrated that As rapidly and selectively blocks the transcription of NF-B-dependent genes in HTLV-I infected cells only. Reversal by As alone of NF-B activation resulted from dramatic stabilization of IB- and IB- , independently of IKK activity modulation or Tax degradation. In contrast, only the As/IFN combination induced late and massive down-regulation of cell-cycle regulated genes, concomitantly with Tax degradation by the proteasome and cell death induction, indicating the importance of continuous Tax expression for ATL cell survival. These two successive events likely account for the potent and specific effects of the As/IFN combination in ATL.
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