Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression

Oncol Rep. 2008 Nov;20(5):1093-7.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Cell Cycle Proteins
  • Cell Line, Tumor
  • Down-Regulation
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • Methylnitronitrosoguanidine / toxicity
  • Nuclear Proteins / biosynthesis
  • Nuclear Proteins / drug effects*
  • Nuclear Proteins / genetics
  • Oligonucleotide Array Sequence Analysis
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • Rosiglitazone
  • Stomach Neoplasms / drug therapy*
  • Stomach Neoplasms / metabolism*
  • Thiazolidinediones / pharmacology*
  • Up-Regulation

Substances

  • Antineoplastic Agents
  • Cell Cycle Proteins
  • Commd5 protein, rat
  • Nuclear Proteins
  • Thiazolidinediones
  • Rosiglitazone
  • Methylnitronitrosoguanidine