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miRNA-126 inhibits proliferation, migration and invasion of human lung cancer A549 cells via EGFR/AKT/mTOR pathway / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 458-463, 2016.
Artigo em Chinês | WPRIM | ID: wpr-490665
ABSTRACT

AIM:

To investigate the effects of microRNA ( miRNA)-126 on the proliferation , migration and in-vasion of human lung cancer cell lines , and to explore its mechanism .

METHODS:

The A549 cells were transfected with miRNA-126 agomir by Lipofectamine 2000.The expression of miRNA-126 was detected by real-time PCR.The cell activity was detected by MTT assay .The number of viable A549 cells was counted by the method of Trypan blue exclusion .The cell colony-forming capability was determined by cell colony formation test .The cell migration and invasion abilities were assayed by wound healing and Transwell methods , respectively.The protein levels of p-EGFR, EGFR, p-AKT, AKT, p-mTOR and mTOR were determined by Western blot .

RESULTS:

The expression level of miRNA-126 was significantly in-creased in the A549 cells compared with negative control ( NC) group and control group ( P<0.01 ) .The proliferation of A549 cells was decreased extremely after transfected with the miRNA-126 agomir (P<0.01), so did the result of the cell colony-formation test.The migration and invasion abilities of the lung cancer cells were also significantly inhibited .The protein levels of p-EGFR, p-AKT and p-mTOR were significantly down-regulated compared with NC group and control group ( P<0.01) .

CONCLUSION:

Over-expression of miRNA-126 significantly inhibits the proliferation , migration and invasion ability of human lung cancer A 549 cells by down-regulation of EGFR/AKT/mTOR pathway .

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo