Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression

被引：13
作者：
Chen, Bai-Li [3 ]
Yu, Jun [2 ]
Zeng, Zhi-Rong [3 ]
Chu, Wai-Kit [2 ]
Wong, Christine Y. P. [2 ]
Cheng, Yuen-Yee [2 ]
Sung, Joseph J. Y. [2 ]
Hu, Pin-Jin [3 ]
Leung, Wai K. [1 ,2 ]
机构：
[1] Chinese Univ Hong Kong, Dept Med & Therapeut, Inst Digest Dis, Shatin, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Shatin, Hong Kong, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Gastroenterol, Guangzhou 510275, Guangdong, Peoples R China
来源：
ONCOLOGY REPORTS | 2008年 / 20卷 / 05期
关键词：
rosiglitazone; peroxisome proliferator-activated receptors;
D O I：
10.3892/or_00000114
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Our previous study demonstrated that PPAR gamma ligand rosiglitazone prevents gastric carcinogenesis in rats induced by chemical carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). In this study, we attempted to identify novel anticancer mechanisms of rosiglitazone. By examining the gene expression profiles of MNNG-induced and rosiglitazone-treated gastric cancer with Uniset Rat I Bioarray microarray, we identified a gene that showed prominent responses in the rosiglitazone-treated group. The hypertension-related, calcium-regulated gene (HCaRG) was significantly up-regulated in rat gastric carcinoma of the rosiglitazone-treated group when compared with the MNNG group. We further examined HCaRG expression in human gastric cancer and found that the expression of HCaRG was down-regulated in human gastric cancerous tissue. Rosiglitazone markedly induced the expression of HCaRG in the AGS cell line. The up-regulation of HCaRG may be one of the mechanisms underlying the chemopreventive effect of rosiglitazone in gastric cancer.
引用
收藏
页码：1093 / 1097
页数：5
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