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Prepublished online as a Blood First Edition Paper on December 27, 2002; DOI 10.1182/blood-2002-06-1770.
Submitted June 14, 2002
Accepted December 17, 2002
TNF-related apoptosis-inducing ligand (TRAIL) frequently induces apoptosis in Philadelphia chromosome-positive leukemia cells
Kanako Uno, Takeshi Inukai*, Nobuhiko Kayagaki, Kumiko Goi, Hiroki Sato, Atsushi Nemoto, Kazuya Takahashi, Keiko Kagami, Noriko Yamaguchi, Hideo Yagita, Ko Okumura, Toshiko Koyama-Okazaki, Toshio Suzuki, Kanji Sugita, and Shinpei Nakazawa
Department of Pediatrics, University of Yamanashi, School of Medicine, Yamanashi, Japan
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan
Laboratory of Immunology, Saitama Shakaihoken Hospital, Saitama, Japan
* Corresponding author; email: tinukai{at}res.yamanashi-med.ac.jp.
TNF-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL) have been implicated in anti-tumor immunity and therapy. In the present study, we investigated the sensitivity of Philadelphia chromosome (Ph1)-positive leukemia cell lines to TRAIL- or FasL-induced cell death to explore the possible contribution of these molecules to immunotherapy against Ph1-positive leukemias. TRAIL, but not FasL, effectively induced apoptotic cell death in most of five chronic myelogenous leukemia (CML)-derived and seven acute leukemia (AL)-derived Ph1-positive cell lines. The sensitivity to TRAIL was correlated with cell surface expression of death-inducing receptors DR4 and/or DR5. The TRAIL-induced cell death was caspase-dependent and enhanced by NF- B inhibitors. Moreover, primary leukemia cells from Ph1-positive ALL patients were also sensitive to TRAIL, but not to FasL, depending on DR4/DR5 expression. FADD and caspase-8, components of death-inducing signaling complex (DISC), as well as FLIP, a negative regulator of caspase-8, were expressed ubiquitously in Ph1-positive leukemia cell lines irrespective of their differential sensitivities to TRAIL and FasL. Notably, TRAIL could induce cell death in the Ph1-positive leukemia cell lines that were refractory to a BCR-ABL-specific tyrosine kinase inhibitor STI571. These results suggested the potential utility of recombinant TRAIL as a novel therapeutic agent and the possible contribution of endogenously expressed TRAIL to immunotherapy against Ph1-positive leukemias.
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