期刊
LEUKEMIA
卷 28, 期 11, 页码 2165-2177出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2014.120
关键词
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资金
- National Center for Research Resources [5P20RR018757-10]
- National Institute of General Medical Sciences [8P20GM103414-10]
The basis for persistence of leukemic stem cells in the bone marrow microenvironment remains poorly understood. We present evidence that signaling cross-talk between alpha 4 integrin and Abelson interactor-1 (Abi-1) is involved in the acquisition of an anchorage-dependent phenotype and drug resistance in Bcr-Abl-positive leukemia cells. Comparison of Abi-1 (ABI-1) and alpha 4 integrin (ITGA4) gene expression in relapsing Bcr-Abl-positive CD34 + progenitor cells demonstrated a reduction in Abi-1 and an increase in alpha 4 integrin mRNA in the absence of Bcr-Abl mutations. This inverse correlation between Abi-1 and alpha 4 integrin expression, as well as linkage to elevated phospho-Akt and phospho-Erk signaling, was confirmed in imatinib mesylate -resistant leukemic cells. These results indicate that the alpha 4-Abi-1 signaling pathway may mediate acquisition of the drug-resistant phenotype of leukemic cells.
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