Laboratory of Gastroenterology, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, Zhejiang Province 310009, China.
Cancer Lett. 2013 Feb 28;329(2):155-63. doi: 10.1016/j.canlet.2012.10.038. Epub 2012 Nov 8.
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.
异常的胞质分裂增加了肿瘤细胞核融合的可能性。然而，微小 RNA（miRNA）在异常胞质分裂中的作用尚不清楚。在这里，我们发现 miR-1290 在临床结肠癌组织中显著上调。miR-1290 的上调延迟了胞质分裂，导致多核细胞的形成。KIF13B 是 miR-1290 的靶标，参与了异常的胞质分裂。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。
