کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2113588 | 1084479 | 2011 | 10 صفحه PDF | دانلود رایگان |

We investigated the effect of a novel Wnt/β-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 T315I mutation-harboring cells. AV65 reduced the expression of β-catenin in CML cells, resulting in the induction of apoptosis. Moreover, AV65 inhibited the proliferation of hypoxia-adapted primitive CML cells that overexpress β-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.
► AV65 is a novel Wnt/β-catenin signaling inhibitor.
► AV65 inhibited the proliferation of CML cell including T315I-mutated cells.
► AV65 also inhibited the proliferation of hypoxia-adapted primitive CML cells.
► AV65 inhibited the CML cell proliferation in combination with imatinib.
Journal: Cancer Letters - Volume 312, Issue 1, 15 December 2011, Pages 91–100