Background
It is well known that nuclear factor of activated T cells c1 (NFATc1) expression is closely associated with progression of many cancers. And we found that miR-338 could directly target the NFATc1. However, the precise mechanisms of miR-338 in non-small-cell lung cancer (NSCLC) have not been well clarified. Our study aimed to explore the interaction between NFATc1 and miR-338 in NSCLC.
Conclusions
Overexpression of miR-338 inhibited cell proliferation and EMT of NSCLC cells by directly down-regulating NFATc1 expression.
Methods
Quantitative RT-PCR was utilized to determine the expressions of NFATc1 and miR-338 in NSCLC tissues and cell lines. And the cell proliferation and epithelial-mesenchymal transition (EMT) were assessed to determine the functional roles of miR-338 and NFATc1 in NSCLC cells. NFATc1 expression was detected using quantitative RT-PCR and western blotting, respectively. Luciferase reporter assays were performed to validate NFATc1 as a target of miR-338 in NSCLC cells.
Results
In this study, our results showed that NFATc1 expression was significantly up-regulated in NSCLC tissues and cell lines, and the miR-338 level was dramatically down-regulated. Moreover high NFATc1 expression was closely associated with low miR-338 level in NSCLC tissues. Moreover introduction of miR-338 significantly inhibited proliferation and EMT of NSCLC cells. Bioinformatics analysis predicted that the NFATc1 was a potential target gene of miR-338. We demonstrated that miR-338 could directly target NFATc1 by using luciferase reporter assay. Besides, knockdown of NFATc1 had the similar effects with miR-338 overexpression on NSCLC cells. Up-regulation of NFATc1 in NSCLC cells partially abolished the inhibitory effects of miR-338 mimic. Conclusions: Overexpression of miR-338 inhibited cell proliferation and EMT of NSCLC cells by directly down-regulating NFATc1 expression.