| Summary: | <p>Abstract</p> <p>Background</p> <p>Although current chemotherapy regimens have remarkably improved the cure rate of pediatric acute promyelocytic leukemia (APL) over the past decade, more than 20% of patients still die of the disease, and the 5-year cumulative incidence of relapse is 17%. The precise gene pathways that exert critical control over the determination of cell lineage fate during the development of pediatric APL remain unclear.</p> <p>Methods</p> <p>In this study, we analyzed <it>miR-125b </it>expression in 169 pediatric acute myelogenous leukemia (AML) samples including 76 APL samples before therapy and 38 APL samples after therapy. The effects of enforced expression of <it>miR-125b </it>were evaluated in leukemic cell and drug-resistant cell lines.</p> <p>Results</p> <p><it>miR-125b </it>is highly expressed in pediatric APL compared with other subtypes of AML and is correlated with treatment response, as well as relapse of pediatric APL. Our results further demonstrated that <it>miR-125b </it>could promote leukemic cell proliferation and inhibit cell apoptosis by regulating the expression of tumor suppressor BCL2-antagonist/killer 1 (Bak1). Remarkably, <it>miR-125b </it>was also found to be up-regulated in leukemic drug-resistant cells, and transfection of a <it>miR-125b </it>duplex into AML cells can increase their resistance to therapeutic drugs,</p> <p>Conclusions</p> <p>These findings strongly indicate that <it>miR-125b </it>plays an important role in the development of pediatric APL at least partially mediated by repressing BAK1 protein expression and could be a potential therapeutic target for treating pediatric APL failure.</p>
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