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微小RNA-96下调RECK以促进非小细胞肺癌细胞的生长和运动能力。

MiR-96 downregulates RECK to promote growth and motility of non-small cell lung cancer cells.

作者信息

Guo Haizhou, Li Qianping, Li Weihao, Zheng Tianliang, Zhao Song, Liu Zhangsuo

机构信息

Department of thoracic surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.

出版信息

Mol Cell Biochem. 2014 May;390(1-2):155-60. doi: 10.1007/s11010-014-1966-x. Epub 2014 Jan 29.

Abstract

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.

摘要

微小RNA在非小细胞肺癌(NSCLC)的发生和发展中起关键作用。miR-96在某些恶性肿瘤中作为癌基因发挥作用,但其在NSCLC中的作用尚不清楚。在此,我们证实miR-96在人NSCLC组织和细胞系中均显著上调。抑制miR-96表达可显著降低NSCLC细胞的增殖、集落形成、迁移和侵袭能力。富含半胱氨酸的Kazal基序逆转诱导蛋白(RECK)被确定为NSCLC细胞中miR-96的靶标。此外,在NSCLC组织中发现RECK的表达与miR-96的表达呈负相关。我们的数据表明,miR-96可能通过靶向RECK部分促进NSCLC细胞的生长和运动。

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