Effects of PPVI on Apoptosis and Autophagy of Esophageal Cancer Cells ECA-109 by Regulating PI3K/AKT/mTOR Pathway
Objective:To investigate the effects of saponin Ⅵ(PPVI)on apoptosis and autophagy of esophageal cancer cells by regulating PI3K/AKT/mTOR pathway.Methods:ECA-109 cells were divided into control(no treatment),PPVI low-dose group(PPVI treatment added 2.5mg/L),PPVI medium-dose group(PPVI treatment added 5.0mg/L),PPVI high-dose group(PPVI treatment added 7.5mg/L),IGF-1 group(IGF-1 added 10 mg/L)nmol/mL IGF-1 treatment),IGF-1+PPVI group(10 nmol/mL IGF-1 and 7.5mg/L PPVI treatment were added),CCK-8 was used to detect ECA-109 cell viability,Transwell was used to detect ECA-109 cell migration.Apoptosis of ECA-109 cells was detected by flow cytometry,and PI3K/AKT/mTOR signaling pathway.Results:The proliferation activity of ECA-109 cells in low-dose PPVI,medium-dose PPVI and high-dose,and the apoptosis increased(P＜0.001),while the proliferation activity and migration ECA-109 cells in IGF-1 increased.The apoptosis capacity was significantly decreased(P＜0.001).Compared with PPVI high-dose,proliferation activity and migration ability of ECA-109 cells in IGF-1+PPVI increased,and apoptosis ability was significantly decreased(P＜0.001).The protein levels of P-PI3K,P-Akt,P-mTOR and LC3B Ⅱ/Ⅰ in ECA-109 cells of PPVI low,PPVI medium and PPVI high decreased,while the protein p62 were significantly increased(P＜0.001).The protein levels of P-PI3K,P-Akt,P-mTOR and LC3B Ⅱ/Ⅰ in ECA-109 cells of IGF-1 were significantly increased,while p62 decreased(P＜0.001).PPVI high-dose,the protein levels of P-PI3K,P-Akt,P-MTOR and LC3B Ⅱ/Ⅰ in ECA-109 cells of IGF-1+PPVI increased,while the protein p62 were significantly decreased(P＜0.001).Conclusions:PPVI may induce apoptosis and autophagy of ECA-109 cells by inhibiting PI3K/AKT/mTOR pathway,and inhibit pro-liferation and migration of ECA-109 cells.
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维普
