BACKGROUND: : Acute myeloid leukemia (AML) is the most common malignancy of the bone marrow with a high mortality. Recent advances in high-throughput sequencing have led to the identification of various miRNAs implicated in the pathogenesis of AML. We found in this study that miR-650, a miRNA that was traditionally considered to participate in the onset of hepatocellular carcinoma, might play a significant role in AML development and progression. METHODS: : qRT-PCR was used to detect the expression of miR-650 and Gfi1 in AML patients and healthy controls. Next, a luciferase assay was conducted to verify the target effect of miR-650 on Gfi1. Moreover, the CCK-8 assay was performed to evaluate the effect of miR-650 on the proliferation of AML cells in the presence and absence of Gfi1. RESULTS: : miR-650 was downregulated in AML whereas Gfi1 was upregulated. miR-650 could negatively regulate Gfi1 via direct targeting of its 3'-UTR, which was confirmed by luciferase assay. In addition, overexpression of miR-650 reduced cell proliferation in K562 cells, whereas an increase in cell proliferation was observed when K562 cells were transfected with miR-650 inhibitor, which was compromised in response to the knockdown of Gfi1. CONCLUSIONS: : Our research demonstrated that miR-650 modulates cell proliferation in AML through affecting the expression of Gfi1, which occurs by direct target action.
BACKGROUND: : Acute myeloid leukemia (AML) is the most common malignancy of the bone marrow with a high mortality. Recent advances in high-throughput sequencing have led to the identification of various miRNAs implicated in the pathogenesis of AML. We found in this study that miR-650, a miRNA that was traditionally considered to participate in the onset of hepatocellular carcinoma, might play a significant role in AML development and progression. METHODS: : qRT-PCR was used to detect the expression of miR-650 and Gfi1 in AMLpatients and healthy controls. Next, a luciferase assay was conducted to verify the target effect of miR-650 on Gfi1. Moreover, the CCK-8 assay was performed to evaluate the effect of miR-650 on the proliferation of AML cells in the presence and absence of Gfi1. RESULTS: : miR-650 was downregulated in AML whereas Gfi1 was upregulated. miR-650 could negatively regulate Gfi1 via direct targeting of its 3'-UTR, which was confirmed by luciferase assay. In addition, overexpression of miR-650 reduced cell proliferation in K562 cells, whereas an increase in cell proliferation was observed when K562 cells were transfected with miR-650 inhibitor, which was compromised in response to the knockdown of Gfi1. CONCLUSIONS: : Our research demonstrated that miR-650 modulates cell proliferation in AML through affecting the expression of Gfi1, which occurs by direct target action.