151. Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
- Author
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Christine Y. P. Wong, Wai Kit Chu, Pinjin Hu, Jun Yu, Wai K. Leung, Zhirong Zeng, Baili Chen, Yuen Yee Cheng, and Joseph J.Y. Sung
- Subjects
chemistry.chemical_classification ,Cancer Research ,medicine.medical_specialty ,Oncogene ,business.industry ,Cancer ,Peroxisome proliferator-activated receptor ,General Medicine ,medicine.disease ,medicine.disease_cause ,Molecular medicine ,Endocrinology ,Oncology ,chemistry ,Internal medicine ,Gene expression ,medicine ,Cancer research ,Rosiglitazone ,business ,Stomach cancer ,Carcinogenesis ,medicine.drug - Abstract
Our previous study demonstrated that PPARgamma 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 anti-cancer 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.
- Published
- 1994