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 Blood, 15 January 2006, Vol. 107, No. 2, pp. 679-688.
Prepublished online as a Blood First Edition Paper on October 4, 2005; DOI 10.1182/blood-2005-05-1982.

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NEOPLASIA

Dihydroflavonol BB-1, an extract of natural plant Blumea balsamifera, abrogates TRAIL resistance in leukemia cells

Hiroo Hasegawa, Yasuaki Yamada, Kanki Komiyama, Masahiko Hayashi, Masami Ishibashi, Tatsushi Yoshida, Toshiyuki Sakai, Takashi Koyano, Toh-Seok Kam, Ken Murata, Kazuyuki Sugahara, Kazuto Tsuruda, Norihiko Akamatsu, Kunihiro Tsukasaki, Masato Masuda, Nobuyuki Takasu, and Shimeru Kamihira

From the Department of Laboratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki; Kitasato Institute, Tokyo; Kitasato Institute for Life Sciences, Kitasato University, Tokyo; Graduate School of Pharmaceutical Sciences, Chiba University, Chiba; Department of Molecular-Targeting, Cancer Prevention, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto; Temko Corporation, Tokyo; Department of Hematology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki; Second Department of Internal Medicine, University of the Ryukyus, Okinawa, Japan; and Department of Chemistry, University of Malaysia, Kuala Lumpur, Malaysia.

Tumor necrosis factor (TNF)–related apoptosis-inducing ligand (TRAIL) induces apoptosis in many transformed cells but not in normal cells and, hence, has emerged as a novel anticancer agent. Previously, we showed that although most adult T-cell leukemia/lymphoma (ATLL) cells express the TRAIL death receptor DR4 (TRAIL-R1) or DR5 (TRAIL-R2), they are resistant to TRAIL. Thus, in this study, we tried to find natural products that can overcome TRAIL resistance. Among more than 150 materials screened, a dihydroflavonol that was extracted from Blumea balsamifera (BB-1) exhibited the most striking synergism with TRAIL. Treatment of the TRAIL-resistant ATLL cell line KOB, with a combination of BB-1 and TRAIL, resulted in apparent apoptosis that was not observed on treatment with either agent alone. Furthermore, pretreatment with BB-1 followed by TRAIL further augmented the synergism. BB-1 increased the level of TRAIL-R2 promoter activity and surface protein expression in a p53-independent manner. TRAIL-R2 siRNA inhibited the synergism, indicating that sensitization was caused by the increase of TRAIL-R2 expression. More interestingly, similar effects were observed in other leukemia cell lines by exactly the same mechanisms. These results suggest that combined treatment with BB-1 and TRAIL may be a new strategy for cancer therapy.


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