Journal
CANCER LETTERS
Volume 312, Issue 1, Pages 91-100Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2011.08.002
Keywords
beta-Catenin; CML; Imatinib-resistance; T315I; Hypoxia-adaptation
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Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan (Center for Frontier Medicine)
- Yasuda Medical Foundation
- Fujiwara Memorial Foundation
- Grants-in-Aid for Scientific Research [21590443, 21390293, 23591404, 21591246, 23592678] Funding Source: KAKEN
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We investigated the effect of a novel Wnt/beta-catenin signaling inhibitor, AV65 on imatinib mesylate (IM)-sensitive and -resistant human chronic myeloid leukemia (CML) cells in vitro. AV65 inhibited the proliferation of various CML cell lines including 1315I mutation-harboring cells. AV65 reduced the expression of beta-catenin in CML cells, resulting in the induction of apoptosis. Moreover, AV65 inhibited the proliferation of hypoxia-adapted primitive CML cells that overexpress beta-catenin. The combination of AV65 with IM had a synergistic inhibitory effect on the proliferation of CML cells. These findings suggest that AV65 could be a novel therapeutic agent for the treatment of CML (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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