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Article: Rosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
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TitleRosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
 
AuthorsChen, BL1
Yu, J2
Zeng, ZR1
Chu, WK2
Wong, CYP2
Cheng, YY2
Sung, JJY2
Hu, PJ1
Leung, WK2
 
Issue Date2008
 
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
 
CitationOncology Reports, 2008, v. 20 n. 5, p. 1093-1097 [How to Cite?]
DOI: http://dx.doi.org/10.3892/or_00000114
 
AbstractOur previous study demonstrated that PPARγ 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 rosiglitazonetreated 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 upregulated 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.
 
ISSN1021-335X
2013 Impact Factor: 2.191
2013 SCImago Journal Rankings: 0.935
 
DOIhttp://dx.doi.org/10.3892/or_00000114
 
ISI Accession Number IDWOS:000260648200014
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChen, BL
 
dc.contributor.authorYu, J
 
dc.contributor.authorZeng, ZR
 
dc.contributor.authorChu, WK
 
dc.contributor.authorWong, CYP
 
dc.contributor.authorCheng, YY
 
dc.contributor.authorSung, JJY
 
dc.contributor.authorHu, PJ
 
dc.contributor.authorLeung, WK
 
dc.date.accessioned2012-09-05T05:28:52Z
 
dc.date.available2012-09-05T05:28:52Z
 
dc.date.issued2008
 
dc.description.abstractOur previous study demonstrated that PPARγ 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 rosiglitazonetreated 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 upregulated 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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationOncology Reports, 2008, v. 20 n. 5, p. 1093-1097 [How to Cite?]
DOI: http://dx.doi.org/10.3892/or_00000114
 
dc.identifier.doihttp://dx.doi.org/10.3892/or_00000114
 
dc.identifier.epage1097
 
dc.identifier.isiWOS:000260648200014
 
dc.identifier.issn1021-335X
2013 Impact Factor: 2.191
2013 SCImago Journal Rankings: 0.935
 
dc.identifier.issue5
 
dc.identifier.pmid18949406
 
dc.identifier.scopuseid_2-s2.0-58149329042
 
dc.identifier.spage1093
 
dc.identifier.urihttp://hdl.handle.net/10722/163220
 
dc.identifier.volume20
 
dc.languageeng
 
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/OR/or.htm
 
dc.publisher.placeGreece
 
dc.relation.ispartofOncology Reports
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshAntineoplastic Agents - Pharmacology
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshDown-Regulation
 
dc.subject.meshGene Expression
 
dc.subject.meshHumans
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshMethylnitronitrosoguanidine - Toxicity
 
dc.subject.meshNuclear Proteins - Biosynthesis - Drug Effects - Genetics
 
dc.subject.meshOligonucleotide Array Sequence Analysis
 
dc.subject.meshRats
 
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
 
dc.subject.meshStomach Neoplasms - Drug Therapy - Metabolism
 
dc.subject.meshThiazolidinediones - Pharmacology
 
dc.subject.meshUp-Regulation
 
dc.titleRosiglitazone suppresses gastric carcinogenesis by up-regulating HCaRG expression
 
dc.typeArticle
 
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<contributor.author>Cheng, YY</contributor.author>
<contributor.author>Sung, JJY</contributor.author>
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<description.abstract>Our previous study demonstrated that PPAR&#947; ligand rosiglitazone prevents gastric carcinogenesis in rats induced by chemical carcinogen N-methyl-N&apos;-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 rosiglitazonetreated 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 upregulated 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.</description.abstract>
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Author Affiliations
  1. Sun Yat-Sen University
  2. Chinese University of Hong Kong