miR-145 and miR-497 suppress TGF-β-induced epithelial-mesenchymal transition of non-small cell lung cancer by targeting MTDH
- PMID: 30065618
- PMCID: PMC6062944
- DOI: 10.1186/s12935-018-0601-4 (V体育官网)
miR-145 and miR-497 suppress TGF-β-induced epithelial-mesenchymal transition of non-small cell lung cancer by targeting MTDH (V体育官网)
Abstract
Background: MicroRNAs (miRNAs) have been reported to play crucial roles in multiple cancers including non-small cell lung cancer (NSCLC) VSports手机版. Here, we investigated the role of miR-145 and miR-497 in TGF-β-induced epithelial-mesenchymal transition (EMT) process of NSCLC. .
Methods: We performed quantitative real time PCR (qRT-PCR) to detect the expression level of miR-145 and miR-497 in NSCLC cell lines. Then in the presence/absence of TGF-β, we transfected miRNA mimics or inhibitor into A549 and H1299 cells and investigated the role of miR-145 and miR-497 in cell migration and invasion using transwell and wound-healing assay. The regulation role of miR-145 and miR-497 on Metadherin (MTDH) was determined by luciferase assay V体育安卓版. The expression level of MTDH and EMT markers E-cadherin and vimentin were detected on mRNA and protein level. .
Results: In our study, our results showed that miR-145 and miR-497 were downregulated in NSCLC cell lines. Overexpression of miR-145 and miR-497 inhibited TGF-β-induced EMT and suppressed cancer cell migration and invasion, while the opposite results were observed in cells transfected with miR-145 or miR-497 inhibitor. Moreover, the luciferase assay confirmed that miR-145 and miR-497 attenuated MTDH expression by directly binding 3'-UTR of MTDH mRNA and exert the tumor-suppression role V体育ios版. .
Conclusions: Overall, we demonstrated that miR-145 and miR-497 functioned as EMT-suppressor in NSCLC by targeting MTDH, provided new evidence that miR-145 and miR-497 as potential therapeutic targets VSports最新版本. .
Keywords: Epithelial–mesenchymal transition; MTDH; Non-small cell lung cancer; miR-145; miR-497 V体育平台登录. .
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