miR-96 downregulates RECK to promote growth and motility of non-small cell lung cancer cells
miR-96 downregulates RECK to promote growth and motility of non-small cell lung cancer cells
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DOI：
10.1007/s11010-014-1966-x
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发表时间：
2014-05-01
影响因子：
4.3
通讯作者：
Liu, Zhangsuo
中科院分区：
文献类型：
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作者：
Guo, Haizhou;Li, Qianping;Liu, Zhangsuo
MicroRNA在非小细胞肺癌（NSCLC）的发生和发展中起着关键作用。miR-96在某些恶性肿瘤中作为致癌基因发挥作用，而其在NSCLC中的作用尚不清楚。在这里，我们验证了miR-96在人类NSCLC组织和细胞系中均显著增加。抑制miR-96表达显著降低了NSCLC细胞的细胞增殖、集落形成、迁移和侵袭。具有kazal基序的逆转诱导富含半胱氨酸蛋白（RECK）被鉴定为NSCLC细胞中miR-96的靶点。RECK与miR-96在NSCLC组织中的表达呈负相关。我们的数据表明，miR-96可能部分通过靶向RECK促进NSCLC细胞的生长和运动。
MicroRNAs play critical roles in the development and progression of non-small cell lung cancer (NSCLC). miR-96 acts as an oncogene in some malignancies, while its role in NSCLC is unclear. Here, we validated that miR-96 was significantly increased in both human NSCLC tissues and cell lines. Inhibition of miR-96 expression remarkably reduced cell proliferation, colony formation, migration, and invasion of NSCLC cells. Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) was identified as a target of miR-96 in NSCLC cells. In addition, the expression of RECK was found to be negatively correlated with the expression of miR-96 in NSCLC tissues. Our data suggest that miR-96 might promote the growth and motility of NSCLC cells partially by targeting RECK.