Solasonine promotes apoptosis of non-small cell lung cancer cells by regulating the Bcl-2/Bax/caspase-3 pathway
10.12122/j.issn.1673-4254.2024.06.11
- VernacularTitle:澳洲茄碱通过调控Bcl-2/Bax/caspase-3信号通路促进非小细胞肺癌发生凋亡
- Author:
Guiling CHEN
1
;
Xiaofeng LIAO
;
Pengtao SUN
;
Huan CEN
;
Shengchun SHU
;
Bijing LI
;
Jinhua LI
Author Information
1. 广州中医药大学第二附属医院,广东 广州 510120
- Keywords:
solasonine;
lung cancer;
Bcl-2/Bax/caspase-3 signaling pathway;
homologous phosphatase tensin protein;
apoptosis
- From:
Journal of Southern Medical University
2024;44(6):1109-1116
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of solasonine,an active component of Solanum nigrum,on proliferation and apoptosis of non-small cell lung cancer PC9 cells.Methods PC9 cells were treated with 2,5,10,15,20,or 25 μmol/L solasonine,and the changes in cell proliferation were examined using CCK-8 assay.Tetramethyl rhodamine ethyl ester(TMRE)was used to detect the changes in mitochondrial membrane potential,and caspase-3/7 detection kit and GreenNuc? caspase-3/Annexin V-mCherry kit for live cell were used to analyze the changes in caspase-3 of the cells.Annexin V-FITC/PI double staining was employed to analyze the apoptosis rate of the cells.The effect of PTEN inhibitors on solasonine-induced cell apoptosis was examined by detecting apoptosis-related protein expressions using Western blotting.Results Solasonine treatment for 24,48,and 72 h significantly lowered the viability of PC9 cells.The cells treated with solasonine for 24 h showed significantly decreased mitochondrial membrane potential and increased cell apoptosis with enhanced caspase-3/7 and caspase-3 activities and expression of cleaved caspase-3.Solasonine treatment significantly decreased phosphorylation levels of PI3K and Akt,increased the protein expressions of PTEN and Bax,and lowered the expression of Bcl-2 protein in the cells.Conclusion Solasonine inhibits proliferation and induces apoptosis of PC9 cells by regulating the Bcl-2/Bax/caspase-3 pathway and its upstream proteins.