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首页> 外文期刊>Cell biology international. >MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim.
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MiR-92a mediates AZD6244 induced apoptosis and G1-phase arrest of lymphoma cells by targeting Bim.

机译：MiR-92A通过靶向BIM介导AZD6244诱导淋巴瘤细胞的诱导细胞凋亡和G1相阻滞。

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摘要

AZD6244, an ATP-uncompetitive inhibitor of mitogen-activated protein kinase 1/2 (MEK1/2), has shown activity in several malignant tumours. However, whether AZD6244 has a function in lymphoma cells is not known. We report that AZD6244 treatment represses the growth of Raji and MOLT4 cells by inducing apoptosis and G1-phase arrest. Using miRNAs array and quantitative RT-PCR, miR-92a was downregulated byAZD6244 treatment through the ERK1/2-AP1 signalling pathway. Overexpression of miR-92a abrogated AZD6244-induced apoptosis and G1-phase arrest, indicating that it is involved in the cytotoxicity of AZD6244 in lymphoma cells. A luciferase reporter assay showed that miR-92a directly targetsthe 3'-UTRs of Bim. Overexpression of miR-92a mimics downregulated Bim mRNA and protein expression level, indicating that miR-92a negatively regulates its expression at both levels. Silencing Bim decreases AZD6244-induced apoptosis and G1-phase arrest, suggesting that Bim contributes to the growth arrest. Thus, miR-92a mediates AZD6244-induced cytotoxicity of lymphoma cells by targeting Bim. Downregulation of miR-92a by AZD6244 is mediated by the ERK1/2-AP1 signalling pathway.
机译：AZD6244是丝裂型促乳丝糖苷活化蛋白激酶1/2（MEK1 / 2）的ATP非竞争性抑制剂，在几种恶性肿瘤中显示出活性。然而，AZD6244是否具有淋巴瘤细胞中的功能是未知的。我们认为AZD6244治疗通过诱导细胞凋亡和G1相阻止抑制RAJI和MOLT4细胞的生长。使用MiRNAS阵列和定量RT-PCR，MiR-92a通过ERK1 / 2-AP1信号通路进行了通过ERK1 / 2-AP1信号通路进行了处理。 MiR-92a的过度表达废除AZD6244诱导的细胞凋亡和G1相阻滞，表明它参与AZD6244在淋巴瘤细胞中的细胞毒性。荧光素酶报告器测定显示MIR-92a直接靶向BIM的3'-UTR。 miR-92a模拟的过表达下调的BIM mRNA和蛋白质表达水平，表明miR-92a负调节其在两个水平的表达。沉默BIM降低AZD6244诱导的细胞凋亡和G1相逮捕，表明BIM有助于增长逮捕。因此，MiR-92A通过靶向BIM介导淋巴瘤细胞的细胞毒性诱导的淋巴瘤细胞毒性。 AZD6244的MiR-92a的下调由ERK1 / 2-AP1信号通路介导。

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