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Effects of quercetin on suppressing migration and invasion of A549 cells via the STAT3 signaling pathway / 国际药学研究杂志
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-845395
Biblioteca responsável: WPRO
ABSTRACT
Objective To investigate the effect of quercetin on suppressing the proliferation, migration and invasion of A549 cells via the signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods The A549 cells were cultured in vitro and treated with quercetin at various concentrations (0,7.5,15,30,60 and 120 µmol/L) for 24 h,48 h and 72 h. The proliferation of A549 and the 50% inhibitory concentration (IC50) were measured by the cell counting kit-8 (CCK-8). The A549 cells treated for 24 h were randomly divided into 4 groups the blank control, 15 and 30 µmol/L quercetin, and 3 µg/ml cisplatin(the positive control) groups. The effect of quercetin on adhesion rate was detected by the cell adhesion assay; the cell migration ability was evaluated by the wound healing assay; the cell invasion ability was evaluated by the Transwell chamber assay; the expression of STAT3 and phosphorylated-STAT3 (p-STAT3) proteins were detected by Western blot assay. Results Quercetin inhibited A549 cell growth dose-dependently. Compared with the blank control group, quercetin could significantly inhibit the adhesion rate, migration ability and invasion of A549 cells (P<0.05 or P<0.01); compared with the blank control group, quercetin significantly inhibited STAT3 and p-STAT3 expression level (P<0.05 or P<0.01). Conclusion Quercetin could inhibit the proliferation, migration and invasion of A549 cells, and the mechanism is libely related to the STAT3 signal pathway.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of International Pharmaceutical Research Ano de publicação: 2017 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Journal of International Pharmaceutical Research Ano de publicação: 2017 Tipo de documento: Artigo
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