File Download
  • No File Attached
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Promoter hypermethylation mediates downregulation of thiamine receptor SLC19A3 in gastric cancer
  • Basic View
  • Metadata View
  • XML View
TitlePromoter hypermethylation mediates downregulation of thiamine receptor SLC19A3 in gastric cancer
 
AuthorsLiu, X1
Lam, EKY1
Wang, X2
Zhang, J1
Cheng, YY1
Lam, YW2
Ng, EKO1
Yu, J1
Chan, FKL1
Jin, H1
Sung, JJY1
 
KeywordsGastric cancer
Methylation
SLC19A3
 
Issue Date2009
 
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
 
CitationTumor Biology, 2009, v. 30 n. 5-6, p. 242-248 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000243767
 
AbstractAs an important way to inactivate tumor suppressor genes (TSGs) during cancer development, promoter hypermethylation can be used to define novel TSGs and identify biomarkers for cancer diagnosis. SLC19A3 (solute carrier family 19, member 3) was found to be such a biomarker. SLC19A3 expression was downregulated in gastric cancer cell lines (71%, 5/7) and restored after pharmacological demethylation. Notably, hypermethylation of SLC19A3 promoter was detected in gastric cancer cell lines (57%, 4/7), primary gastric carcinoma tissues (51%, 52/101) and precancerous lesion (intestinal metaplasia) tissues (32%, 8/25). Exogenous SLC19A3 expression caused growth inhibition of gastric cancer cells. In summary, SLC19A3 was epigenetically downregulated in gastric cancer. Methylation of SLC19A3 promoter could be a novel biomarker for early gastric cancer development. © 2009 S. Karger AG, Basel.
 
ISSN1010-4283
2012 Impact Factor: 2.518
2012 SCImago Journal Rankings: 0.813
 
DOIhttp://dx.doi.org/10.1159/000243767
 
ISI Accession Number IDWOS:000272106800002
Funding AgencyGrant Number
Institute of Digestive Disease
Chinese University of Hong Kong2007.1.034
Funding Information:

The project was supported by Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong and CUHK direct grant (2007.1.034).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLiu, X
 
dc.contributor.authorLam, EKY
 
dc.contributor.authorWang, X
 
dc.contributor.authorZhang, J
 
dc.contributor.authorCheng, YY
 
dc.contributor.authorLam, YW
 
dc.contributor.authorNg, EKO
 
dc.contributor.authorYu, J
 
dc.contributor.authorChan, FKL
 
dc.contributor.authorJin, H
 
dc.contributor.authorSung, JJY
 
dc.date.accessioned2010-09-17T10:34:47Z
 
dc.date.available2010-09-17T10:34:47Z
 
dc.date.issued2009
 
dc.description.abstractAs an important way to inactivate tumor suppressor genes (TSGs) during cancer development, promoter hypermethylation can be used to define novel TSGs and identify biomarkers for cancer diagnosis. SLC19A3 (solute carrier family 19, member 3) was found to be such a biomarker. SLC19A3 expression was downregulated in gastric cancer cell lines (71%, 5/7) and restored after pharmacological demethylation. Notably, hypermethylation of SLC19A3 promoter was detected in gastric cancer cell lines (57%, 4/7), primary gastric carcinoma tissues (51%, 52/101) and precancerous lesion (intestinal metaplasia) tissues (32%, 8/25). Exogenous SLC19A3 expression caused growth inhibition of gastric cancer cells. In summary, SLC19A3 was epigenetically downregulated in gastric cancer. Methylation of SLC19A3 promoter could be a novel biomarker for early gastric cancer development. © 2009 S. Karger AG, Basel.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationTumor Biology, 2009, v. 30 n. 5-6, p. 242-248 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000243767
 
dc.identifier.doihttp://dx.doi.org/10.1159/000243767
 
dc.identifier.epage248
 
dc.identifier.hkuros168714
 
dc.identifier.isiWOS:000272106800002
Funding AgencyGrant Number
Institute of Digestive Disease
Chinese University of Hong Kong2007.1.034
Funding Information:

The project was supported by Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong and CUHK direct grant (2007.1.034).

 
dc.identifier.issn1010-4283
2012 Impact Factor: 2.518
2012 SCImago Journal Rankings: 0.813
 
dc.identifier.issue5-6
 
dc.identifier.openurl
 
dc.identifier.pmid19816091
 
dc.identifier.scopuseid_2-s2.0-73749088408
 
dc.identifier.spage242
 
dc.identifier.urihttp://hdl.handle.net/10722/92056
 
dc.identifier.volume30
 
dc.languageeng
 
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
 
dc.publisher.placeSwitzerland
 
dc.relation.ispartofTumor Biology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshCell Survival - genetics
 
dc.subject.meshDNA Methylation
 
dc.subject.meshMembrane Transport Proteins - genetics
 
dc.subject.meshPromoter Regions, Genetic - genetics
 
dc.subject.meshStomach Neoplasms - genetics - pathology
 
dc.subjectGastric cancer
 
dc.subjectMethylation
 
dc.subjectSLC19A3
 
dc.titlePromoter hypermethylation mediates downregulation of thiamine receptor SLC19A3 in gastric cancer
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Liu, X</contributor.author>
<contributor.author>Lam, EKY</contributor.author>
<contributor.author>Wang, X</contributor.author>
<contributor.author>Zhang, J</contributor.author>
<contributor.author>Cheng, YY</contributor.author>
<contributor.author>Lam, YW</contributor.author>
<contributor.author>Ng, EKO</contributor.author>
<contributor.author>Yu, J</contributor.author>
<contributor.author>Chan, FKL</contributor.author>
<contributor.author>Jin, H</contributor.author>
<contributor.author>Sung, JJY</contributor.author>
<date.accessioned>2010-09-17T10:34:47Z</date.accessioned>
<date.available>2010-09-17T10:34:47Z</date.available>
<date.issued>2009</date.issued>
<identifier.citation>Tumor Biology, 2009, v. 30 n. 5-6, p. 242-248</identifier.citation>
<identifier.issn>1010-4283</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/92056</identifier.uri>
<description.abstract>As an important way to inactivate tumor suppressor genes (TSGs) during cancer development, promoter hypermethylation can be used to define novel TSGs and identify biomarkers for cancer diagnosis. SLC19A3 (solute carrier family 19, member 3) was found to be such a biomarker. SLC19A3 expression was downregulated in gastric cancer cell lines (71%, 5/7) and restored after pharmacological demethylation. Notably, hypermethylation of SLC19A3 promoter was detected in gastric cancer cell lines (57%, 4/7), primary gastric carcinoma tissues (51%, 52/101) and precancerous lesion (intestinal metaplasia) tissues (32%, 8/25). Exogenous SLC19A3 expression caused growth inhibition of gastric cancer cells. In summary, SLC19A3 was epigenetically downregulated in gastric cancer. Methylation of SLC19A3 promoter could be a novel biomarker for early gastric cancer development. &#169; 2009 S. Karger AG, Basel.</description.abstract>
<language>eng</language>
<publisher>S Karger AG. The Journal&apos;s web site is located at http://www.karger.com/TBI</publisher>
<relation.ispartof>Tumor Biology</relation.ispartof>
<subject>Gastric cancer</subject>
<subject>Methylation</subject>
<subject>SLC19A3</subject>
<subject.mesh>Cell Survival - genetics</subject.mesh>
<subject.mesh>DNA Methylation</subject.mesh>
<subject.mesh>Membrane Transport Proteins - genetics</subject.mesh>
<subject.mesh>Promoter Regions, Genetic - genetics</subject.mesh>
<subject.mesh>Stomach Neoplasms - genetics - pathology</subject.mesh>
<title>Promoter hypermethylation mediates downregulation of thiamine receptor SLC19A3 in gastric cancer</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=1010-4283&amp;volume=30&amp;issue=5-6&amp;spage=242&amp;epage=248&amp;date=2009&amp;atitle=Promoter+hypermethylation+mediates+downregulation+of+thiamine+receptor+SLC19A3+in+gastric+cancer</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1159/000243767</identifier.doi>
<identifier.pmid>19816091</identifier.pmid>
<identifier.scopus>eid_2-s2.0-73749088408</identifier.scopus>
<identifier.hkuros>168714</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-73749088408&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>30</identifier.volume>
<identifier.issue>5-6</identifier.issue>
<identifier.spage>242</identifier.spage>
<identifier.epage>248</identifier.epage>
<identifier.isi>WOS:000272106800002</identifier.isi>
<publisher.place>Switzerland</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. City University of Hong Kong