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Article: Fibulin 1 is downregulated through promoter hypermethylation in gastric cancer

TitleFibulin 1 is downregulated through promoter hypermethylation in gastric cancer
Authors
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
Citation
British Journal Of Cancer, 2008, v. 99 n. 12, p. 2083-2087 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/92222
ISSN
2014 Impact Factor: 4.836
2014 SCImago Journal Rankings: 2.205
PubMed Central ID
ISI Accession Number ID
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.

References

 

DC FieldValueLanguage
dc.contributor.authorCheng, YYen_HK
dc.contributor.authorJin, Hen_HK
dc.contributor.authorLiu, Xen_HK
dc.contributor.authorSiu, JMTen_HK
dc.contributor.authorWong, YPen_HK
dc.contributor.authorNg, EKOen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorLeung, WKen_HK
dc.contributor.authorSung, JJYen_HK
dc.contributor.authorChan, FKLen_HK
dc.date.accessioned2010-09-17T10:39:40Z-
dc.date.available2010-09-17T10:39:40Z-
dc.date.issued2008en_HK
dc.identifier.citationBritish Journal Of Cancer, 2008, v. 99 n. 12, p. 2083-2087en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92222-
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.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectFBLN1en_HK
dc.subjectGastric canceren_HK
dc.subjectMethylationen_HK
dc.subjectTumour suppressor geneen_HK
dc.titleFibulin 1 is downregulated through promoter hypermethylation in gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.emailNg, EKO: ngko@hku.hken_HK
dc.identifier.emailLeung, WK: waikleung@hku.hken_HK
dc.identifier.authorityNg, EKO=rp01364en_HK
dc.identifier.authorityLeung, WK=rp01479en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/sj.bjc.6604760en_HK
dc.identifier.pmid18985039en_HK
dc.identifier.pmcidPMC2607230-
dc.identifier.scopuseid_2-s2.0-57449097981en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-57449097981&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume99en_HK
dc.identifier.issue12en_HK
dc.identifier.spage2083en_HK
dc.identifier.epage2087en_HK
dc.identifier.eissn1532-1827-
dc.identifier.isiWOS:000261620100016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheng, YY=7404914973en_HK
dc.identifier.scopusauthoridJin, H=24577511700en_HK
dc.identifier.scopusauthoridLiu, X=36062536700en_HK
dc.identifier.scopusauthoridSiu, JMT=14008789500en_HK
dc.identifier.scopusauthoridWong, YP=24802808500en_HK
dc.identifier.scopusauthoridNg, EKO=21135553700en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridLeung, WK=7201504523en_HK
dc.identifier.scopusauthoridSung, JJY=35405352400en_HK
dc.identifier.scopusauthoridChan, FKL=7202586434en_HK
dc.identifier.citeulike3481157-

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