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Prepublished online as a Blood First Edition Paper on January 30, 2003; DOI 10.1182/blood-2002-09-2986.
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Blood, 1 June 2003, Vol. 101, No. 11, pp. 4576-4582
NEOPLASIA
Arsenic/interferon specifically reverses 2 distinct gene networks critical for the survival of HTLV-1–infected leukemic cells
Rihab Nasr,
Andreas Rosenwald,
Marwan E. El-Sabban,
Bertrand Arnulf,
Pierre Zalloua,
Yves Lepelletier,
Françoise Bex,
Olivier Hermine,
Louis Staudt,
Hugues de Thé, and
Ali Bazarbachi
From the Departments of Internal Medicine, Biochemistry and Human Morphology, American University of Beirut, Beirut, Lebanon; Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD; CNRS URA 1461 and Department of Hematology, Necker Hospital, Paris, France; Chronic Care Center, Baabda, Lebanon; Departement de Biologie Moléculaire, Université Libre de Bruxelles, Brussels, Belgium; and UPR 9051 CNRS, Laboratoire Associé au Comité de Paris de la Ligue contre le Cancer, Paris, France.
Adult T-cell leukemia (ATL) is a severe chemotherapy-resistant malignancy associated with prolonged infection by the human T cell-lymphotropic virus 1 (HTLV-1) 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. Because arsenic trioxide (As) and interferon  (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-1–infected leukemic cells. The As/IFN combination reduced Tax expression and, accordingly, reversed the Tax-induced constitutive nuclear factor  B (NF-B) activation. Using DNA microarray analyses, we demonstrated that As rapidly and selectively blocks the transcription of NF-B–dependent genes in HTLV-1–infected cells only. Reversal of NF-B activation by As alone resulted from dramatic stabilization of IB- and IB- , independently of IB kinase (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 2 successive events likely account for the potent and specific effects of the As/IFN combination in ATL.
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