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miR-145 and miR-497 suppress TGF-β-induced epithelial–mesenchymal transition of non-small cell lung cancer by targeting MTDH

Authors
  • Yin, Qi1
  • Han, Yang2
  • Zhu, Dongyi1
  • Li, Zhanxia3
  • Shan, Shan4
  • Jin, Wenjing5
  • Lu, Qingchun1
  • Ren, Tao1, 4
  • 1 Tongji University School of Medicine, Department of Respiratory Medicine, Shanghai East Hospital, Shanghai, 200120, China , Shanghai (China)
  • 2 Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Department of Pathology, Shanghai, 200233, China , Shanghai (China)
  • 3 Tongji University School of Medicine, Department of Intensive Care Unit, Shanghai East Hospital, Shanghai, 200120, China , Shanghai (China)
  • 4 Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Department of Respiratory Medicine, Shanghai, 200233, China , Shanghai (China)
  • 5 Fudan University Pudong Medical Center, Department of Intensive Care Unit, Shanghai Pudong Hospital, Shanghai, 201399, China , Shanghai (China)
Type
Published Article
Journal
Cancer Cell International
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jul 27, 2018
Volume
18
Issue
1
Identifiers
DOI: 10.1186/s12935-018-0601-4
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundMicroRNAs (miRNAs) have been reported to play crucial roles in multiple cancers including non-small cell lung cancer (NSCLC). Here, we investigated the role of miR-145 and miR-497 in TGF-β-induced epithelial–mesenchymal transition (EMT) process of NSCLC.MethodsWe 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. The expression level of MTDH and EMT markers E-cadherin and vimentin were detected on mRNA and protein level.ResultsIn 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.ConclusionsOverall, 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.

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