MicroRNA-193b regulates c-Kit proto-oncogene and represses cell proliferation in acute myeloid leukemia
MicroRNA-193b regulates c-Kit proto-oncogene and represses cell proliferation in acute myeloid leukemia
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MicroRNA-193b 调节 c-Kit 原癌基因并抑制急性髓系白血病细胞增殖
DOI：
10.1016/j.leukres.2011.06.010
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发表时间：
2011-09-01
影响因子：
2.7
通讯作者：
Yu, Li
中科院分区：
文献类型：
--
作者：
Gao, Xiao-ning;Lin, Ji;Yu, Li
c-Kit原癌基因的突变和/或过表达经常发生在急性髓性白血病（AML）的亚群中，并导致异常细胞增殖和不良结局。我们发现，c-Kit的表达受到microRNA（miRNA）-193b的转录后调控。值得注意的是，miR-193b在检查的AML细胞中显著下调，其水平与c-Kit水平呈负相关。AML细胞中miR-193b表达的恢复导致c-Kit表达明显降低并抑制细胞生长。这些数据揭示了miR-193b失调在髓系白血病发生中的作用以及调节miR-193b表达对c-Kit阳性AML的治疗前景。(C)2011爱思唯尔有限公司保留所有权利。
Mutations and/or overexpression of c-Kit proto-oncogene frequently occur in subsets of acute myeloid leukemia (AML) and contribute to abnormal cell proliferation and poor outcomes. We showed that c-Kit expression was subject to post-transcriptional regulation by microRNA (miRNA)-193b. Notably, miR-193b was significantly down-regulated in the examined AML cells and its levels were inversely correlated with c-Kit levels. Restoration of miR-193b expression in AML cells resulted in distinctly reduced c-Kit expression and inhibited cell growth. These data reveal a role for miR-193b dysregulation in myeloid leukemogenesis and the therapeutic promise of regulating miR-193b expression for c-Kit-positive AML. (C) 2011 Elsevier Ltd. All rights reserved.