Hong Zhao - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Fei Liu - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Ruichun Jia - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Huiying Chang - Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Haixia Li - Department of Ultrasonography, Harbin medical university cancer hospital, Harbin, Heilongjiang ۱۵۰۰۸۱, China
Meijuan Miao - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Hui Wang - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China
Zhiping Yang - Department of Blood Transfusion, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang ۱۵۰۰۰۱, China

Objective(s): Chronic myelogenous leukemia (CML) is a chronic myeloproliferative disorder characterized by the accumulation of myeloid cells with a chromosomal translocation known as the Philadelphia chromosome. In this study, we investigated the roles of miR-۵۷۰ in CML development. Materials and Methods: Expression of miR-۵۷۰ in CML samples and cell lines was determined by qRT-PCR. Glucose uptake and ATP concentration detection assays were used to analyze cell glucose metabolism. MTT and western blot assays were performed for cell proliferation and apoptosis, respectively. The targets of miR-۵۷۰ were predicted by bioinformatics and confirmed using luciferase activity, qRT-PCR and western blot assays. Results: The expression levels of miR-۵۷۰ were significantly reduced in CML clinical samples and cells. Overexpression of miR-۵۷۰ inhibited cell proliferation, promoted apoptosis, and suppressed glucose metabolism in CML cells. Insulin receptor substrates (IRS) ۱ and IRS۲ were identified as direct targets of miR-۵۷۰. IRS۱ or IRS۲ were knocked down in K۵۶۲ cells.Loss of IRS۱/۲ expression led to suppressed cell proliferation, elevated apoptosis, and decreased glucose metabolism in CML cells, which is consistent with their roles as miR-۵۷۰ targets. Conclusion: MiR-۵۷۰ directly targeted IRS۱ and IRS۲ in CML, suppressing cell proliferation and glucose metabolism. MiR-۵۷۰ may provide a strategy for CML therapy.

Chronic myelogenous leukemia, IRS۱, IRS۲, miR-۵۷۰