Effects of β-sitosterol on proliferation and apoptosis of colon cancer cell HCT116
10.3969/j.issn.1673-9701.2024.09.019
- VernacularTitle:β-谷甾醇对结肠癌细胞HCT116增殖和凋亡的影响
- Author:
Xi CHEN
1
;
Ruonan LI
1
;
Jing LI
1
;
Lina ZHAO
1
;
Zhili XU
1
Author Information
1. College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian 116600, Liaoning, China
- Publication Type:Journal Article
- Keywords:
β-sitosterol;
Colon cancer;
Proliferation;
Apoptosis;
Signaling pathway
- From:
China Modern Doctor
2024;62(9):78-81,85
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of β-sitosterol on the proliferation and apoptosis of colon cancer cell HCT116,and its regulation of on phosphoinositide 3-kinase/protein kinase B(PI3K/Akt)signaling pathway.Methods Cultivated colon cancer cells HCT116 in vitro and divided them into β-sitosterol High(240μmol/L)、medium(120μmol/L)and low-dose(60μmol/L)groups,set control group(0μmol/L).Applied different concentrations of β-sitosterol treatment of HCT116 cells.And 24h later,the cell proliferation and activity were determined by cell counting kit-8(CCK-8)method,the morphological changes observed under a microscope;Cell apoptosis was observed by Hoechst 33342 nuclear staining;Used cell colony formation assy to detect the colony forming ability of HCT116 cells;and Western blot was used to evaluate the expression of PI3K,p-Akt,Akt,Bcl-2 and Bax in cells.Used AutoDock software for molecular docking of β-sitosterol with Akt and PI3K.Results Compared with the control group,β-sitosterol could inhibit the proliferation of colon cancer HCT116 cells in a concentration dependent manner,inhibit their colony forming ability and promote cell apoptosis and inhibit the expression of p-Akt、PI3K、and Bcl-2 proteins in HCT116 cells and promotes the expression of Bax protein.The binding of β-sitosterol with PI3K and Akt proteins is relatively stable.Conclusion β-sitosterol may regulate the proliferation and apoptosis of HCT116 through inhibiting PI3K/Akt signaling pathway.