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MiR-20a promotes lung tumorigenesis by targeting RUNX3 via TGF-ß signaling pathway.
Qin, X; Wang, X Y; Fei, J W; Li, F H; Han, J; Wang, H X.
Afiliação
  • Qin X; Department of Respiratory Medicine, Yantaishan Hospital, Yantai, China.
  • Wang XY; Department of Clinical Laboratory, Jinan Zhangqiu District Hospital of TCM, Jinan, China.
  • Fei JW; Department of Respiratory Medicine, Yantaishan Hospital, Yantai, China.
  • Li FH; Department of Respiratory Medicine, Yantaishan Hospital, Yantai, China.
  • Han J; Department of Respiratory Medicine, Yantaishan Hospital, Yantai, China.
  • Wang HX; Department of Respiratory Medicine, Yantaishan Hospital, Yantai, China.
J Biol Regul Homeost Agents ; 34(2)2020 Apr 29.
Article em En | MEDLINE | ID: mdl-32347076
ABSTRACT
MiR-20a shows a significant role in the development of various human tumors. However, its specific biological function in non-small-cell lung cancer (NSCLC) is still not clear. qRT-PCR was applied for detecting miR-20a expression. The analysis of cell growth and apoptosis were performed by MTT, xenograft models, Western blot assays. Dual luciferase reporter, Western blotting and qRT-PCR were carried out to verify the potential target of miR-20a. In NSCLC tissues and cells, miR-20a was highly expressed and RUNX3 was lowly expressed. Moreover, up-regulation of miR-20a expression promoted NSCLC cell proliferation, invasion and migration, while low-expression of miR-20a showed the converse case on cell proliferation, invasion and migration. RUNX3 was verified as the direct target of miR-20a and it could overturn its biological function in NSCLC cells. Moreover, miR-20a negatively regulated RUNX3 expression. Mechanistically, increasing miR-20a expression inhibited RUNX3 expression and then activated the TGF-ß signaling pathway. Taken together, our results demonstrated that re-expression of miR-20a promoted lung tumorigenesis by down-regulation of RUNX3 and facilitating the activation of TGF-ß signaling pathway.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2020 Tipo de documento: Article