Inhibition of lupinol on the malignant progression of lung cancer A549 cells through regulating Notch signaling pathway
10.12173/j.issn.1008-049X.202403208
- VernacularTitle:羽扇豆醇可能通过调控Notch信号通路抑制肺癌A549细胞恶性进展
- Author:
Bingyi YIN
1
;
Hongsheng LIN
;
Chuchu ZHANG
Author Information
1. 中国中医科学院广安门医院肿瘤科(北京 100053)
- Keywords:
Lupeol;
Notch signaling pathway;
Lung cancer cell;
Proliferation;
Apoptosis;
Migration;
Invasion
- From:
China Pharmacist
2024;27(6):961-968
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of lupinol on the proliferation,apoptosis,migration and invasion of lung cancer cells through regulating Notch signaling pathway.Methods Lung cancer cells A549 were cultured in vitro,and the cells were treated with lupeol at concentrations of 0,15,30,and 60 mg/L,with 0 mg/L being the control group and the rese being the lupeol dosage groups,the cells were treated with lupinol at the concentration of 60 mg/L and Notch pathway inhibitor DAPT at the concentration of 10 μmol/L,which was recorded as the lupeol+DAPT group.Cell proliferation changes were detected by MTT;cell apoptosis was detected by flow cytometry;cell migration and invasion were detected by Transwell;protein expression of PCNA,Bcl-2,N-cadherin,E-cadherin,Notch-1 and Hes-1 were detected by Western blot.Results 15,30,60 mg/L lupeol group can significantly inhibit the cell viability,the number of migration cells and invading cells of lung cancer cells,significantly increase the rate of cell apoptosis,and reduce PCNA,N-cadherin,Bcl-2,Hes-1 and Notch-1 expression,increase E-cadherin expression(P<0.05).Compared with the lupeol group,the lupeol+DAPT group significantly reduced cell viability,the number of migrating cells and invaded cells,increased apoptosis rate,decreased PCNA,Bcl-2,Hes-1,Notch-1 and N-cadherin protein expression,and increased E-cadherin protein expression(P<0.05).Conclusion Lupinol may inhibit the invasion,migration and proliferation of lung cancer cells through Notch signaling pathway,and induce apoptosis.