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10.1186/s12935-018-0601-4

http://scihub22266oqcxt.onion/10.1186/s12935-018-0601-4
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C6062944!6062944!30065618
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suck abstract from ncbi


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pmid30065618      Cancer+Cell+Int 2018 ; 18 (ä): ä
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  • miR-145 and miR-497 suppress TGF-?-induced epithelial?mesenchymal transition of non-small cell lung cancer by targeting MTDH #MMPMID30065618
  • Yin Q; Han Y; Zhu D; Li Z; Shan S; Jin W; Lu Q; Ren T
  • Cancer Cell Int 2018[]; 18 (ä): ä PMID30065618show ga
  • Background: MicroRNAs (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-?-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-?, 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. 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-?-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. 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.
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