Mechanism of miR-138/sirt-1 axis on proliferation and metastasis of non-small cell lung cancer

2019 
Objective To investigate the mechanism of microRNA138 (miR-138)/silence information regulator1 (sirt-1) on proliferation and metastasis of non-small cell lung cancer (NSCLC). Methods Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expression of sirt-1 on NSCLC tissues and adjacent tissues.After NSCLC cell lines A549 and H1299 were selected and transfected with empty plasmid, miR-138 mimics and miR-138 inhibitor by lipo3000, the experiment was divided into negative control group, miR-138 group and miR-138 inhibition group.The relation between miR-138 and sirt-1 was evaluated by dual luciferase reporter assay, RT-qPCR and Western blot; the effect of miR-138 on the proliferation of A549 and H1299 were detected by Cell Counting Kit-8 and EdU; the effect of miR-138 on the migration and invasion was detected by Wound-healing and Transwell assays; the expression of epithelial-mesenchymal transition markers including E-cadherin and Vimentin were detected by Western blot. Results The expression of sirt-1 on mRNA level was obviously increased in NSCLC tissues, compared to adjacent tissues.Dual luciferase reporter assay showed the luciferase activity on cotransfection of miR-138 mimics+ sirt-1 wildtype plasmid was lower than others.The expression of sirt-1 in miR-138 group was decreased and that in miR-138 inhibition group was increased, compared to negative control group.The proliferation and metastasis of NSCLC cells in miR-138 group were decreased and those in miR-138 inhibition group were increased, compared to negative control group.The expression of E-cadherin in A549 was increased and the expression of Vimentin in both cell lines were decreased in miR-138 group, compared to negative control group.When miR-138 was inhibited, the result was completely opposite. Conclusions miR-138 suppresses the proliferation and metastasis of NSCLC by regulating sirt-1, which indicates that miR-138/sirt-1 might be a potential therapeutic target for NSCLC. Key words: Silence information regulator-1; Epithelial-to-mesenchymal; microRNA-138; Carcinoma, non-small-cell lung
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