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Article: Fibulin 1 is downregulated through promoter hypermethylation in gastric cancer
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TitleFibulin 1 is downregulated through promoter hypermethylation in gastric cancer
 
AuthorsCheng, YY2
Jin, H2
Liu, X2
Siu, JMT2
Wong, YP2
Ng, EKO2
Yu, J2
Leung, WK2
Sung, JJY2
Chan, FKL2 1
 
KeywordsFBLN1
Gastric cancer
Methylation
Tumour suppressor gene
 
Issue Date2008
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
 
CitationBritish Journal Of Cancer, 2008, v. 99 n. 12, p. 2083-2087 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.bjc.6604760
 
AbstractTumour suppressor genes (TSGs) were frequently inactivated through promoter hypermethylation in gastric carcinoma as well as pre-malignant gastric lesions, suggesting that promoter hypermethylation can be used as a marker to define novel TSGs and also biomarkers for early detection of gastric cancer. In an effort to search for such genes aberrantly methylated in gastric cancer development, fibulin 1 (FBLN1) was found as a candidate TSG epigenetically downregulated in gastric cancer. FBLN1 expression was downregulated in all of gastric cancer cell lines used (100%, 7 out of 7) and the primary gastric carcinoma tissues (84%, 86 out of 102) and significantly restored after pharmacological demethylation. Hypermethylation of the FBLN1 promoter was frequently (71%, 5 out of 7) detected in gastric cancer cell lines and primary gastric carcinoma tissues. Ectopic expression of FBLN1 led to the growth inhibition of gastric cancer cells through the induction of apoptosis. In summary, FBLN1 was identified as a novel candidate TSG epigenetically downregulated in gastric cancer. © 2008 Cancer Research.
 
ISSN0007-0920
2013 Impact Factor: 4.817
 
DOIhttp://dx.doi.org/10.1038/sj.bjc.6604760
 
PubMed Central IDPMC2607230
 
ISI Accession Number IDWOS:000261620100016
Funding AgencyGrant Number
Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong
Funding Information:

The project was supported by Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorCheng, YY
 
dc.contributor.authorJin, H
 
dc.contributor.authorLiu, X
 
dc.contributor.authorSiu, JMT
 
dc.contributor.authorWong, YP
 
dc.contributor.authorNg, EKO
 
dc.contributor.authorYu, J
 
dc.contributor.authorLeung, WK
 
dc.contributor.authorSung, JJY
 
dc.contributor.authorChan, FKL
 
dc.date.accessioned2010-09-17T10:39:40Z
 
dc.date.available2010-09-17T10:39:40Z
 
dc.date.issued2008
 
dc.description.abstractTumour suppressor genes (TSGs) were frequently inactivated through promoter hypermethylation in gastric carcinoma as well as pre-malignant gastric lesions, suggesting that promoter hypermethylation can be used as a marker to define novel TSGs and also biomarkers for early detection of gastric cancer. In an effort to search for such genes aberrantly methylated in gastric cancer development, fibulin 1 (FBLN1) was found as a candidate TSG epigenetically downregulated in gastric cancer. FBLN1 expression was downregulated in all of gastric cancer cell lines used (100%, 7 out of 7) and the primary gastric carcinoma tissues (84%, 86 out of 102) and significantly restored after pharmacological demethylation. Hypermethylation of the FBLN1 promoter was frequently (71%, 5 out of 7) detected in gastric cancer cell lines and primary gastric carcinoma tissues. Ectopic expression of FBLN1 led to the growth inhibition of gastric cancer cells through the induction of apoptosis. In summary, FBLN1 was identified as a novel candidate TSG epigenetically downregulated in gastric cancer. © 2008 Cancer Research.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationBritish Journal Of Cancer, 2008, v. 99 n. 12, p. 2083-2087 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.bjc.6604760
 
dc.identifier.citeulike3481157
 
dc.identifier.doihttp://dx.doi.org/10.1038/sj.bjc.6604760
 
dc.identifier.eissn1532-1827
 
dc.identifier.epage2087
 
dc.identifier.isiWOS:000261620100016
Funding AgencyGrant Number
Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong
Funding Information:

The project was supported by Research Funding from the Institute of Digestive Disease, the Chinese University of Hong Kong.

 
dc.identifier.issn0007-0920
2013 Impact Factor: 4.817
 
dc.identifier.issue12
 
dc.identifier.pmcidPMC2607230
 
dc.identifier.pmid18985039
 
dc.identifier.scopuseid_2-s2.0-57449097981
 
dc.identifier.spage2083
 
dc.identifier.urihttp://hdl.handle.net/10722/92222
 
dc.identifier.volume99
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofBritish Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.subjectFBLN1
 
dc.subjectGastric cancer
 
dc.subjectMethylation
 
dc.subjectTumour suppressor gene
 
dc.titleFibulin 1 is downregulated through promoter hypermethylation in gastric cancer
 
dc.typeArticle
 
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<contributor.author>Siu, JMT</contributor.author>
<contributor.author>Wong, YP</contributor.author>
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<description.abstract>Tumour suppressor genes (TSGs) were frequently inactivated through promoter hypermethylation in gastric carcinoma as well as pre-malignant gastric lesions, suggesting that promoter hypermethylation can be used as a marker to define novel TSGs and also biomarkers for early detection of gastric cancer. In an effort to search for such genes aberrantly methylated in gastric cancer development, fibulin 1 (FBLN1) was found as a candidate TSG epigenetically downregulated in gastric cancer. FBLN1 expression was downregulated in all of gastric cancer cell lines used (100%, 7 out of 7) and the primary gastric carcinoma tissues (84%, 86 out of 102) and significantly restored after pharmacological demethylation. Hypermethylation of the FBLN1 promoter was frequently (71%, 5 out of 7) detected in gastric cancer cell lines and primary gastric carcinoma tissues. Ectopic expression of FBLN1 led to the growth inhibition of gastric cancer cells through the induction of apoptosis. In summary, FBLN1 was identified as a novel candidate TSG epigenetically downregulated in gastric cancer. &#169; 2008 Cancer Research.</description.abstract>
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Author Affiliations
  1. Prince of Wales Hospital Hong Kong
  2. Chinese University of Hong Kong