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微小RNA-630靶向LIM只有蛋白3来调节肺癌细胞的生长和转移。

miR-630 targets LMO3 to regulate cell growth and metastasis in lung cancer.

作者信息

Song Ying-Fang, Hong Jing-Fang, Liu De-Ling, Lin Qing-An, Lan Xiao-Peng, Lai Guo-Xiang

机构信息

Department of Pulmonary and Critical Care Medicine, Fuzhou General Hospital of Nanjing Military Command, Dongfang Hospital, Xiamen University Fuzhou, 350025, China.

Department of Neurosurgery, Fuzhou General Hospital of Nanjing Military Command, Dongfang Hospital, Xiamen University Fuzhou, 350025, China.

出版信息

Am J Transl Res. 2015 Jul 15;7(7):1271-9. eCollection 2015.

Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs that play key roles in cancer development and progression. Therefore, the discovery of miRNAs may provide a new and powerful tool for understanding the mechanism of carcinogenesis. In the present study, we aimed to investigate the functional significance of miR-630 and to identify its possible target genes in human non-small cell lung cancer (NSCLC). Our results showed that miR-630 was significantly down-regulated in NSCLC tissues and cell lines. The enforced expression of miR-630 was able to inhibit cell proliferation, migration, and invasion of NSCLC cells. Moreover, our results further revealed that LMO3, a nuclear LIM-only proteins, was identified as a target of miR-630. Restoration of LMO3 remarkably reversed the tumor-suppressive effects of miR-630 on cell proliferation, migration, and invasion in NSCLC cells. Therefore, we demonstrated that miR-630 suppressed the proliferation, migration, and invasion of NSCLC cells by down-regulating LMO3 expression, suggesting miR-630 as a potential therapeutic target for the treatment of human NSCLC in the future.

摘要

微小RNA(miRNA)是一类小的非编码RNA,在癌症的发生和发展中起关键作用。因此,miRNA的发现可能为理解致癌机制提供一种新的有力工具。在本研究中,我们旨在探讨miR-630的功能意义,并确定其在人类非小细胞肺癌(NSCLC)中的潜在靶基因。我们的结果表明,miR-630在NSCLC组织和细胞系中显著下调。miR-630的强制表达能够抑制NSCLC细胞的增殖、迁移和侵袭。此外,我们的结果进一步表明,LMO3(一种仅含核LIM的蛋白)被确定为miR-630的一个靶标。LMO3的恢复显著逆转了miR-630对NSCLC细胞增殖、迁移和侵袭的肿瘤抑制作用。因此,我们证明miR-630通过下调LMO3表达来抑制NSCLC细胞的增殖、迁移和侵袭,提示miR-630在未来可能成为治疗人类NSCLC的潜在治疗靶点。

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