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miR-4792 Inhibits Acute Myeloid Leukemia Cell Proliferation and Invasion and Promotes Cell Apoptosis by Targeting Kindlin-3

机译:miR-4792抑制急性髓性白血病细胞增殖和侵袭,促进indlin-3促进细胞凋亡

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It has been reported that kindlin-3 expression is closely associated with progression of many cancers and microRNA (miRNA) processing. However, the effects and precise mechanisms of kindlin-3 in acute myeloid leukemia (AML) have not been well clarified. Our study aimed to explore the interaction between kindlin-3 and miR-4792 in AML. In our study, we found that the expression of kindlin-3 was dramatically increased in AML samples and cell lines, and the miR-4792 level was significantly downregulated. Interestingly, the low miR-4792 level was closely associated with upregulated kindlin-3 expression in AML samples. Moreover, introduction of miR-4792 dramatically suppressed proliferation and invasion and induced apoptosis of AML cells. We demonstrated that miR-4792 could directly target kindlin-3 by using both bioinformatics analysis and luciferase reporter assay. In addition, kindlin-3 silencing had similar effects with miR-4792 overexpression on AML cells. Overexpression of kindlin-3 in AML cells partially reversed the inhibitory effects of miR-4792 mimic. miR-4792 inhibited cell proliferation and invasion and induced apoptosis of AML cells by directly downregulating kindlin-3 expression, and miR-4792 targeting kindlin-3 was responsible for the regulation of the proliferation, invasion, and apoptosis of AML cells.
机译:据报道,Kindlin-3表达与许多癌症和MicroRNA(miRNA)加工的进展密切相关。然而,Nicein-3在急性髓性白血病(AML)中的效果和精确机制并未澄清。我们的研究旨在探讨Kindlin-3和MiR-4792在AML之间的互动。在我们的研究中,我们发现,在AML样品和细胞系中,Kindlin-3的表达显着增加,MiR-4792水平显着下调。有趣的是,低miR-4792水平与AML样本中的上调肤色-3表达密切相关。此外,引入miR-4792显着抑制了增殖和侵袭并诱导了AML细胞的凋亡。我们证明MIR-4792可以通过使用生物信息学分析和荧光素酶报告器测定来直接靶向林林-3。此外,Kindlin-3沉默对AML细胞的miR-4792过表达具有类似的效果。在AML细胞中的Kindlin-3的过度表达部分反转miR-4792模拟的抑制作用。 MiR-4792通过直接下调Kindlin-3表达抑制细胞增殖和侵袭和诱导AML细胞凋亡,并且靶向Kindlin-3的miR-4792负责调节AML细胞的增殖,侵袭和凋亡。

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