Relationship between the activated status of EGFR signal pathway and the sensitivity of colon carcinoma cells to gefitinib
- VernacularTitle:EGFR信号通路的活化状态与结肠癌细胞对吉非替尼敏感性的关系
- Author:
Li YANG
;
Xiaoxing ZHAO
;
Jianjun LI
;
Houjie LIANG
- Publication Type:Journal Article
- Keywords:
colonic neoplasms;
cell line;
gefitinib;
receptor,epidermal growth factor;
mitogen-activated protein kinases;
PTEN phosphohydrolase;
proto-oncogene proteins c-akt
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the inhibitory effects of gefitinib on the growth of colon carcinoma cells with different degree of sensitivity,and the activated status of epidermal growth factor receptor(EGFR) associated signal pathway proteins.Methods The colon carcinoma cell lines(Lovo,HCT116 and HT29) were treated with 10?mol/L of gefitinib,and flow cytometry was employed to detect the cell cycle and apoptosis.Another portion of cells were treated with 50ng/ml of epidermal growth factor(EGF) or 5?mol/L or 10 ?mol/L of EGF+gefitinib,and Western blotting was used to determine the expressions of PTEN,EGFR,AKT and MAPK,as well as their corresponding phosphorylated proteins,p-EGFR,p-AKT and p-MAPK.Results After being treated with gefitinib,the G1 phase cells and apoptosis rate increased remarkably in Lovo,slightly in HT29,while no significant change was found in HCT116.With the treatment of EGF alone,the expressions of p-EGFR,p-AKT and p-MAPK increased significantly in Lovo and HT29 cells(P0.05).Conclusions The growth of colon carcinoma cells,which are resistant to gefitinib,is not dependent on EGFR,and the activated status of signal pathway of the gefitinib-resistant cells will not be inhibited as the EGFR is blocked.The present findings suggest that sensitivity of colon carcinoma cells to gefitinib relies on EGFR as well as the activation of its downstream signal pathway.
