MiR-186 targets ROCK1 to suppress the growth and metastasis of NSCLC cells
MiR-186 targets ROCK1 to suppress the growth and metastasis of NSCLC cells
复制标题
DOI：
10.1007/s13277-014-2168-6
复制
发表时间：
2014-09-01
期刊：
影响因子：
--
通讯作者：
Zhao, Song
中科院分区：
文献类型：
--
作者：
Cui, Guanghui;Cui, Mingwei;Zhao, Song
微小RNA（miRNAs）在人类癌症中充当癌基因或肿瘤抑制因子。越来越多的证据表明，miRNAs的失调与人类非小细胞肺癌（NSCLC）的发生、发展有关。在这里，我们将miR-186鉴定为NSCLC中的肿瘤抑制因子，其在NSCLC中减少。miR-186的过表达显著抑制NSCLC细胞的增殖、迁移和侵袭。此外，Rho相关蛋白激酶1（ROCK 1）被鉴定为NSCLC细胞中miR-186的靶点。ROCK 1的恢复显著逆转了miR-186对NSCLC细胞增殖、迁移和侵袭的肿瘤抑制作用。此外，ROCK 1与NSCLC中miR-186的表达呈负相关。总的来说，我们的数据表明miR-186通过靶向ROCK 1在NSCLC中发挥肿瘤抑制剂的作用。
MicroRNAs (miRNAs) act as oncogenes or tumor suppressors in human cancers. Increasing evidence shows that deregulation of miRNAs contributes to the development and progression of human non-small cell lung cancer (NSCLC). Here, we identified miR-186 as a tumor suppressor in NSCLC, which was decreased in NSCLC. Overexpression of miR-186 significantly inhibited proliferation, migration, and invasion of NSCLC cells. In addition, Rho-associated protein kinase 1 (ROCK1) was identified as a target of miR-186 in NSCLC cells. Restoration of ROCK1 remarkably reversed the tumor-suppressive effects of miR-186 on cell proliferation, migration, and invasion in NSCLC cells. Furthermore, ROCK1 was inversely correlated with miR-186 expression in NSCLC. Collectively, our data indicate that miR-186 functions as tumor suppressor in NSCLC by targeting ROCK1.