miR-30c的下调通过靶向MTA1促进非小细胞肺癌的侵袭。
Down-regulation of miR-30c promotes the invasion of non-small cell lung cancer by targeting MTA1.
作者信息
Xia Yang, Chen Qiyou, Zhong Zhaopeng, Xu Caihua, Wu Chen, Liu Bin, Chen Yijiang
机构信息
Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu.
出版信息
Cell Physiol Biochem. 2013;32(2):476-85. doi: 10.1159/000354452. Epub 2013 Aug 27.
BACKGROUND
The connection between microRNA expression and lung cancer development has been identified in recent literature. However, the mechanism of microRNA has been poorly elucidated in non-small-cell lung cancer (NSCLC).
METHODS AND RESULTS
Comparing with adjacent tissues (n=75), miR-30c has a lower expression in lung cancer specimens (n=75). The knockdown of miR-30c enhanced the invasion of A549 cells; meanwhile, the overexpression of miR-30c could reverse the effect of the knockdown of miR-30c in vitro. A luciferase assay revealed that miR-30c was directly bound to the 3'-untranslated regions (3'-UTR) of MTA1. QRT-PCR and western blot shows MTA1 was up-regulated in mRNA and protein levels. The effect taken on the invasion of NSCLC by overexpression of MTA1 works the same as down-regulated miR-30c.
CONCLUSION
miR-30c may play a pivotal role in controlling lung cancer invasion through regulating MTA1in NSCLC.
背景
近期文献已证实微小RNA（miRNA）表达与肺癌发展之间存在关联。然而，在非小细胞肺癌（NSCLC）中，miRNA的作用机制尚未完全阐明。
方法与结果
与癌旁组织（n = 75）相比，miR-30c在肺癌组织标本（n = 75）中的表达较低。敲低miR-30c可增强A549细胞的侵袭能力；同时，在体外过表达miR-30c可逆转敲低miR-30c的作用。荧光素酶报告基因检测显示，miR-30c直接与MTA1的3'-非翻译区（3'-UTR）结合。实时定量聚合酶链反应（QRT-PCR）和蛋白质免疫印迹法显示，MTA1的mRNA和蛋白质水平均上调。过表达MTA1对NSCLC侵袭的影响与下调miR-30c相同。
结论
在NSCLC中，miR-30c可能通过调控MTA1在控制肺癌侵袭中发挥关键作用。
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