Department of Clinical Laboratory, Yinzhou People's Hospital, Ningbo 315040, China.
FEBS Lett. 2012 Oct 19;586(20):3761-5. doi: 10.1016/j.febslet.2012.09.016. Epub 2012 Sep 23.
Recent studies have implied that miRNAs act as crucial modulators for epithelial-to-mesenchymal transition (EMT). We found that miR-134 expression correlated with invasive potential and EMT phenotype of NSCLC cells. Functional assays demonstrated that miR-134 inhibited EMT in NSCLC cells. In addition, we showed that Forkhead Box M1 (FOXM1) is a direct target of miR-134. Knockdown of FOXM1 reversed EMT resembling that of miR-134 overexpression. We further found that FOXM1 was involved in TGF-β1-induced EMT in A549 cells. These findings suggest that miR-134 acts as a novel EMT suppressor in NSCLC cells.
最近的研究表明,miRNAs 作为上皮-间充质转化 (EMT) 的关键调节剂发挥作用。我们发现 miR-134 的表达与 NSCLC 细胞的侵袭潜能和 EMT 表型相关。功能分析表明 miR-134 抑制 NSCLC 细胞的 EMT。此外,我们表明 Forkhead Box M1 (FOXM1) 是 miR-134 的直接靶标。FOXM1 的敲低逆转了 EMT,类似于 miR-134 的过表达。我们进一步发现,FOXM1 参与 TGF-β1 诱导的 A549 细胞 EMT。这些发现表明,miR-134 在 NSCLC 细胞中作为一种新型 EMT 抑制剂发挥作用。