Down-regulation of vascular endothelial growth factor by Rosiglitazone in human lung adenocarcinoma cells
- VernacularTitle:罗格列酮下调肺腺癌细胞血管内皮细胞生长因子的表达
- Author:
Fulin ZHAI
;
Yingzhi ZHUANG
;
Jianguo CAO
- Publication Type:Journal Article
- Keywords:
peroxisome proliferators-activated receptor ?;
angiogenesis;
vascular endothelial growth factor;
lung adenocarcinoma
- From:
Chinese Pharmacological Bulletin
2003;0(10):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the role of a peroxisome proliferators-activated receptor gamma ligand,Rosiglitazone,in angiogenesis in human lung adenocarcinoma cells with reference to the regulation of vascular endothelial growth factor(VEGF).Methods Human lung adenocarcinoma A549 cell line was cultured in vitro.Expression of PPAR? and VEGF in A549 lung adenocarcinoma cells treated with different concentrations of Rosiglitazone was examined by semi-quantitative RT-PCR and immunohistochemical staining.Results PPAR? protein levels were higher in cultured A549 cells.RT-PCR and immunohistochemical staining showed that PPAR? mRNA and protein were enhanced in cells treated with Rosiglitazone in a dose-dependent manner,compared with those of untreated cells.Rosiglitazone had a potent inhibitory effect on the expression of VEGF in A549 cells dose-dependently in a range of concentrations.The effect was maximal with 10 ?mol?L~(-1) RSG and weaken over 20 ?mol?L~(-1) RSG,whereas 100 ?mol?L~(-1) RSG didnot have this down-regulation.GW9662,a PPAR? antagonist,partially blocked this effect of Rosiglitazone.Conclusions Activation of PPAR? suppresses angiogenesis in human lung adenocarcinoma.This action is probably associated with the down-regulation of angiogenic factor,VEGF,which may be modulated by PPAR?.These results suggest that PPAR? might be a novel molecular target for angiogenesis lung adenocarcinoma.
