4.6 Article

MiR-940 inhibits TGF-β-induced epithelial-mesenchymal transition and cell invasion by targeting Snail in non-small cell lung cancer

期刊

JOURNAL OF CANCER
卷 10, 期 12, 页码 2735-2744

出版社

IVYSPRING INT PUBL
DOI: 10.7150/jca.31800

关键词

NSCLC; EMT; transforming growth factor beta; microRNA; SNAI1

类别

资金

  1. National Natural Science Foundation of China [81502498, 81802989]
  2. Natural Science Foundation of Jiangsu Province [BK20161224]
  3. Jiangsu Provincial Commission of Health and Family Planning [H201521]
  4. Youth Science and Technology Project of Suzhou Health and Family Planning Commission [KJXW2016016]
  5. Science and Technology Research foundation of Suzhou Municipality [SYS2018063, SYS2018064]

向作者/读者索取更多资源

Increased evidence reveals that miR-940 inhibits the migration and invasion of cancer cells. Considering transforming growth factor beta (TGF-beta) signaling is crucial to cellular epithelial-mesenchymal transition (EMT) process and metastasis of cancer, it is in urgent to explore whether and how miR-940 plays an essential role in regulating TGF-beta-induced EMT in lung cancer progression. In the present study, we observed a reciprocal expression with down-regulated miR-940 and up-regulated Snail mRNA in non-small-cell lung cancer (NSCLC) tissues. we further found that the expression of miR-940 was decreased in NSCLC tissues with lymph node metastasis, advanced TNM stages and poor cell differentiation, in which, on the contrary, the expression of Snail was increased. Overexpression of miR-940 significantly inhibited Snail mRNA and protein expression in A549 and H226 cells. Mechanistically, Snail mRNA was identified as target of miR-940. In addition, miR-940 repressed TGF-beta-induced EMT and further hampered the cell migration and invasion. Finally, siRNA-mediated knockdown of Snail copied the phenotype of miR-940 overexpression in A549 and H226 cells. Taken together, our study reveals that miR-940 can suppress TGF-beta-induced EMT and cell invasion by targeting Snail 3'-UTR mRNA in NSCLC.

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