Combined treatment of 3-hydroxyflavone and imatinib mesylate increases apoptotic cell death of imatinib mesylate- resistant leukemia cells

被引：22
作者：
Kim, Jung-Hyun [1 ,2 ]
Song, Minjung [1 ,2 ]
Kang, Geun-Ho [1 ,2 ]
Lee, Eung-Ryoung [1 ,2 ]
Choi, Hye-Yeon [1 ,2 ]
Lee, Chung [1 ,2 ]
Kim, Jin-Hoi [1 ,2 ]
Kim, Youngsoo [3 ,4 ]
Koo, Bon-Nyeo [5 ]
Cho, Ssang-Goo [1 ,2 ]
机构：
[1] Konkuk Univ, Dept Anim Biotechnol, Seoul, South Korea
[2] Konkuk Univ, Anim Resources Res Ctr, Seoul, South Korea
[3] Seoul Natl Univ, Coll Med, Dept Biomed Sci, Seoul, South Korea
[4] Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea
[5] Yonsei Univ, Coll Med, Anaesthesia & Pain Res Inst, Dept Anaesthesiol & Pain Med, Seoul, South Korea
来源：
LEUKEMIA RESEARCH | 2012年 / 36卷 / 09期
关键词：
Chronic myelogenous leukemia (CML); Flavonoid; 3-Hydroxyflavone; Imatinib mesylate-resistant cells; Phosphor-Bcr/Abl; Apoptosis; CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; IN-VITRO; TYROSINE KINASE; CANCER-THERAPY; CYCLE ARREST; FLAVONOIDS; APIGENIN; GROWTH; INHIBITOR;
D O I：
10.1016/j.leukres.2012.05.018
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Imatinib mesylate, a Bcr/Abl tyrosine kinase inhibitor, is widely used in treating chronic myeloid leukemia. However, drug-resistance of leukemia cells becomes an emergent problem. Herein, various flavonoids were screened for applicability in leukemia treatment, and 3-hydroxyflavone (3-HF) was found to be most effective in reducing cancer cell viability. The combination of 3-HF and imatinib mesylate resulted in significant apoptotic cell death in imatinib mesylate-resistant leukemia cells. Combined treatment resulted in apparent activation of caspases and decrease of the oncoprotein phosphor-Bcr/Abl in leukemia cells. Our results suggest that this combined treatment is beneficial in imatinib mesylateresistant chronic myelogenous leukemia. (c) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码：1157 / 1164
页数：8
相关论文
共 41 条
[1]   Comparison of imatinib, mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen:: high efficacy of drug combinations [J].
Bradeen, Heather A. ;
Eide, Christopher A. ;
O'Hare, Thomas ;
Johnson, Kara J. ;
Willis, Stephanie G. ;
Lee, Francis Y. ;
Druker, Brian J. ;
Deininger, Michael W. .
BLOOD, 2006, 108 (07) :2332-2338
[2]   Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance [J].
Burgess, MR ;
Skaggs, BJ ;
Shah, NP ;
Lee, FY ;
Sawyers, CL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (09) :3395-3400
[3]  
Caltagirone S, 2000, INT J CANCER, V87, P595, DOI 10.1002/1097-0215(20000815)87:4<595::AID-IJC21>3.0.CO
[4]  
2-5
[5]  
Chen JW, 2002, ACTA PHARMACOL SIN, V23, P667
[6]   Genistein inactivates bcl-2, delays the G2/M phase of the cell cycle, and induces apoptosis of human breast adenocarcinoma MCF-7 cells [J].
Constantinou, AI ;
Kamath, N ;
Murley, JS .
EUROPEAN JOURNAL OF CANCER, 1998, 34 (12) :1927-1934
[7]   Flavonoids: Old and new aspects of a class of natural therapeutic drugs [J].
Di Carlo, G ;
Mascolo, N ;
Izzo, AA ;
Capasso, F .
LIFE SCIENCES, 1999, 65 (04) :337-353
[8]   BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571 [J].
Donato, NJ ;
Wu, JY ;
Stapley, J ;
Gallick, G ;
Lin, H ;
Arlinghaus, R ;
Talpaz, M .
BLOOD, 2003, 101 (02) :690-698
[9]   Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. [J].
Druker, BJ ;
Talpaz, M ;
Resta, DJ ;
Peng, B ;
Buchdunger, E ;
Ford, JM ;
Lydon, NB ;
Kantarjian, H ;
Capdeville, R ;
Ohno-Jones, S ;
Sawyers, CL .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (14) :1031-1037
[10]   Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification [J].
Gorre, ME ;
Mohammed, M ;
Ellwood, K ;
Hsu, N ;
Paquette, R ;
Rao, PN ;
Sawyers, CL .
SCIENCE, 2001, 293 (5531) :876-880
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