Study on Apoptosis Mechanism of Human Colon Cancer Cell Lines HCT-1 1 6 Induced by Solasodine
10.14148/j.issn.1672-0482.2016.0069
- VernacularTitle:澳洲茄胺诱导肠癌 HCT-116细胞凋亡的实验研究
- Author:
Yu-Wen ZHUANG
1
;
Jin-Yong ZHOU
;
Jian WU
;
Shen-Lin LIU
Author Information
1. 南京中医药大学第一临床医学院
- Keywords:
Solasodine;
colorectal cancer;
cell apoptosis;
medicine enema
- From:
Journal of Nanjing University of Traditional Chinese Medicine
2017;33(1):69-73
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the effects of Solasodine on the apoptosis of human colon cancer cell line HCT-1 1 6 and the expression of associated genes,and to investigate the mechnism of the inhibition of HCT-1 1 6 cells proliferation.METHODS After treatment,the inhibitory effect of HCT-1 1 6 cell proliferation was determined by Real time non-label cell analyzer. Flow cytometry was employed to detect cell apoptosis.The qPCR method was used to determine the mRNA levels of Bax and Survivin.Protein levels of Bcl-2,Bax,Bcl-xl,Caspase-3,Caspase-8,Caspase-9,PARP,PI3K and Akt were determined by Western blot .RESULTS Real time non-label cell analysis result showed that Solasodine inhibited the growth of HCT-1 1 6 in vitro ,and the potency enhanced with the increase of drug dose and treat time.Flow cytometry found that the cell apoptosis in-creased with the increase of drug concentration.The qPCR showed that the mRNA levels of apoptosis-related genes Bax and Survivin changed.Western blot results revealed that Bax protein levels increased,while Bcl-2 and Bcl-xl protein levels de-creased,and the ratio of Bax/Bcl-2 was also increased.It showed that Solasodine also promoted the Caspase-3,Caspase-8, Caspase-9 and PARP activities,and inhibited the activation of PI3K and Akt .CONCLUSION Solasodine can inhibit HCT-1 1 6 cells proliferation and induce the cell apoptosis via blocking PI3K/Akt signaling pathway and regulating Caspase family,the Bcl-2 family,and the expression of Survivin and PARP.It can regulate these two apoptotic pathways,mitochondrial pathway and death receptor pathway.
