Department of Clinical Laboratory, Yinzhou People's Hospital, Ningbo 315040, China.
Mol Cell Biochem. 2013 Aug;380(1-2):277-82. doi: 10.1007/s11010-013-1682-y. Epub 2013 May 14.
Recent studies have implied that miRNAs act as crucial modulators for epithelial-to-mesenchymal transition (EMT). We found that miR-148a is significantly downregulated in non-small cell lung cancer (NSCLC) compared to adjacent non-cancerous lung tissues, and the downregulated miR-148a was significantly associated with lymph-node metastasis. Functional assays demonstrated that miR-148a inhibited EMT in NSCLC cells. Moreover, miR-148a decreased 3'-untranslated region luciferase activity of ROCK1 and ROCK1 protein expression. Knockdown of ROCK1 reversed EMT resembling that of miR-148a overexpression. Furthermore, ROCK1 was widely upregulated in NSCLC, and its mRNA levels were inversely correlated with miR-148a expression. These findings suggest that miR-148a acts as a novel EMT suppressor in NSCLC cells, at least in part by modulation of ROCK1.
最近的研究表明,miRNAs 作为上皮间质转化 (EMT) 的关键调节剂发挥作用。我们发现,与相邻的非癌性肺组织相比,miR-148a 在非小细胞肺癌 (NSCLC) 中显著下调,下调的 miR-148a 与淋巴结转移显著相关。功能分析表明,miR-148a 抑制 NSCLC 细胞中的 EMT。此外,miR-148a 降低了 ROCK1 的 3'非翻译区荧光素酶活性和 ROCK1 蛋白表达。ROCK1 的敲低逆转了 EMT,类似于 miR-148a 的过表达。此外,ROCK1 在 NSCLC 中广泛上调,其 mRNA 水平与 miR-148a 的表达呈负相关。这些发现表明,miR-148a 在 NSCLC 细胞中作为一种新型 EMT 抑制剂发挥作用,至少部分是通过 ROCK1 的调节。