Long noncoding RNA LINC01186, regulated by TGF-β/SMAD3, inhibits migration and invasion through Epithelial-Mesenchymal-Transition in lung cancer

Accumulating evidence suggests that long noncoding RNAs (lncRNAs) are crucial regulators of the Epithelial-Mesenchymal-Transition (EMT). TGF-β signaling is a major inducer of EMT and can facilitate lung cancer metastasis. However, the role of lncRNAs in this process remains largely unknown. Here, we have identified 291 lncRNAs which were differentially expressed in lung cancer tissues compared with adjacent normal tissues. Of these, the gene body or vicinity of 19 transcripts were also bound by SMAD3. The expression of LINC01186 was significantly decreased in A549 cells treated with TGF-β1. Furthermore, LINC01186 was stably down-regulated in lung cancer tissues compared with normal tissues in TCGA data sets and another published lung cancer data sets. The bioinformatics analysis suggested that LINC01186 was associated with TGF-β and might participate in EMT process. Moreover, knocking-down LINC01186 promoted cell migration and invasion, whereas, LINC01186 overexpression prevented cell metastasis. Importantly, LINC01186 expression was regulated by SMAD3. And LINC01186 affected several EMT markers expression. These findings suggest that LINC01186, a mediator of TGF-β signaling, can play a significant role in the regulation of EMT and lung cancer cell migration and invasion. [Display omitted] •291 lncRNAs were identified as differentially expressed in lung cancer tissues compared with adjacent normal tissues.•Among 291 differentially expressed lncRNAs, the gene body or vicinity of 19 lncRNAs were also bound by SMAD3.•Our data suggest LINC01186 was associated with TGF-β pathway and it functions by influencing several EMT markers expression.•LINC01186 inhibited cell migration, invasion and colony formation.•This is the first study to establish a role of a previously uncharacterized lncRNA in TGF-β induced EMT in lung cancer.