Your browser doesn't support javascript.
loading
Sequoiaflavone inhibits stem cell properties such as proliferation and invasion of gastric cancer cells by down-regulating PI3K/AKT signaling pathway / 中国临床药理学与治疗学
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-1014633
Biblioteca responsável: WPRO
ABSTRACT

AIM:

To explore the molecular mechanism of sequoiaflavone affecting gastric cancer cells. MEHTODS Gastric cancer cell line AGS cells were treated with gradient concentrations of sequoiaflavone, and then induced by PI3K/AKT signaling pathway activator. The optimal inhibitory concentration and time of semi-inhibitory concentration of red cedar flavonoid on AGS cells were detected by CCK-8, and the changes of cell proliferation, migration and invasion ability were detected by colony formation assay, transwell assay and wound healing assay. PI3K/AKT signal pathway related proteins p-PI3K, PI3K, p-AKT and AKT were detected by western blot.

RESULTS:

Sequoiaflavone inhibited AGS cells in a concentration-dependent manner. The half inhibitory concentration was 0.5 mmol/L, the optimal treatment time was 48 h. The protein expression of p-PI3K and p-AKT was down regulated. The proliferation, migration and invasion of AGS cells were decreased after treated with sequoiaflavone. After treated with PI3K / AKT signal pathway activator, the protein expression level of pPI3K and p-AKT was partially reversed, and the ability of cell viability, proliferation, migration and invasion was also partially improved.

CONCLUSION:

Inactivation of PI3K/AKT signaling pathway caused by sequoiaflavone inhibited gastric cancer cells proliferation, migration and invasion ability.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Pharmacology and Therapeutics Ano de publicação: 2023 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Pharmacology and Therapeutics Ano de publicação: 2023 Tipo de documento: Artigo
...