Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells
Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells
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microRNA-1290 的上调会损害胞质分裂并影响结肠癌细胞的重编程
DOI：
10.1016/j.canlet.2012.10.038
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发表时间：
2013-02-28
期刊：
影响因子：
9.7
通讯作者：
Mao, Jianshan
中科院分区：
文献类型：
--
作者：
Wu, Jia;Ji, Xiaowei;Mao, Jianshan
异常胞质分裂增加了肿瘤细胞核融合的可能性。然而，microRNAs（miRNAs）在异常胞质分裂中的作用尚不清楚。在此，我们发现miR-1290在临床结肠癌组织中显著上调。miR-1290的上调推迟了胞质分裂并导致多核细胞的形成。KIF 13 B是参与异常胞质分裂的miR-1290的靶标。此外，miR-1290的强制表达激活了Wnt通路，并增加了重编程相关转录因子c-Myc和Nanog。我们的研究结果表明，结肠癌细胞中miR-1290的上调损害了胞质分裂并影响了重编程。(C)2012爱思唯尔爱尔兰有限公司保留所有权利。
Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming. (C) 2012 Elsevier Ireland Ltd. All rights reserved.