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TGF-?1-induced epithelial?mesenchymal transition in lung cancer cells involves upregulation of miR-9 and downregulation of its target, E-cadherin #MMPMID29118814
Wang H; Wu Q; Zhang Y; Zhang HN; Wang YB; Wang W
Cell Mol Biol Lett 2017[]; 22 (ä): ä PMID29118814show ga
Background: TGF-?1 plays an important role in the epithelial?mesenchymal transition (EMT) of epithelial cancers, including non-small cell lung cancer (NSCLC). While the full underlying mechanism remains unclear, miR-9 is known to play a critical role in the regulation of NSCLC cell invasion. We tested whether miR-9 targets E-cadherin and thus affects TGF-?1-induced EMT in NSCLC cells by assessing the expression levels of miR-9 and E-cadherin for NSCLC patients and then verifying the targeting of E-cadherin by miR-9 using the dual luciferase reporter system. Results: MiR-9 was significantly upregulated in NSCLC tissues compared with its level in adjacent normal tissues. The expression of E-cadherin in NSCLC tissues was significantly decreased. In addition, we found that TGF-?1 significantly upregulated the expression of miR-9 and downregulated the expression of E-cadherin. E-cadherin was confirmed as a direct target gene of miR-9. Using an miR-9 inhibitor reversed the TGF-?1-mediated inhibition of E-cadherin expression and upregulation of the mesenchymal marker ?-SMA. TGF-?1 significantly induced cell invasion, and this effect was significantly inhibited by miR-9 inhibitors. Conclusions: TGF-?1 induced EMT in NSCLC cells by upregulating miR-9 and downregulating miR-9?s target, E-cadherin.