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Article: Inactivation of helicase-like transcription factor by promoter hypermethylation in human gastric cancer

TitleInactivation of helicase-like transcription factor by promoter hypermethylation in human gastric cancer
Authors
Issue Date2003
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/
Citation
Molecular Carcinogenesis, 2003, v. 37 n. 2, p. 91-97 How to Cite?
AbstractHelicase-like transcription factor (HLTF), a member of the SWI/SNF (mating type switching/sucrose nonfermenting) chromatin-remodeling complex, is recently found to be inactivated by promoter hypermethylation in human colorectal cancer. However, the role of this putative tumor suppressor gene in other tumors has not been determined. We evaluated the role of HLTF promoter hypermethylation in gastric cancer. Expression of HLTF was examined by reverse-transcription (RT)-polymerase chain reaction (PCR), and promoter hypermethylation in HLTF was determined by methylation-specific PCR. Bisulfite DNA sequencing was performed to determine the detailed methylation profiles of the promoter region. HLTF expression was lost in two of five gastric cell lines and in 13 (28%) of 46 primary gastric cancers. Accordingly, promoter hypermethylation was detected in the two cell lines and in nine of 13 gastric cancer samples. Of the ten normal gastric specimens and ten paired adjacent nonneoplastic tissues, methylation was detected in only one adjacent nonneoplastic tissue. Bisulfite DNA sequencing of the promoter region of HLTF showed that the CpG island was densely methylated in cell lines and cancer samples; this also appeared to correlate with expression level. Treatment of gastric cell lines that lacked HLTF expression with the demethylating agent 5-azacytidine (5-azaDC) restored HLTF expression. These results suggest that HLTF promoter hypermethylation is frequently demonstrated in human gastric cancer, and inactivation of HLTF or the chromatin-remodeling complex may play a crucial role in gastric carcinogenesis. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/162688
ISSN
2015 Impact Factor: 4.722
2015 SCImago Journal Rankings: 1.393
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorBai, AHCen_US
dc.contributor.authorChan, MWYen_US
dc.contributor.authorChan, KKen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorChan, FKLen_US
dc.contributor.authorNg, EKWen_US
dc.contributor.authorChung, SCSen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:22:23Z-
dc.date.available2012-09-05T05:22:23Z-
dc.date.issued2003en_US
dc.identifier.citationMolecular Carcinogenesis, 2003, v. 37 n. 2, p. 91-97en_US
dc.identifier.issn0899-1987en_US
dc.identifier.urihttp://hdl.handle.net/10722/162688-
dc.description.abstractHelicase-like transcription factor (HLTF), a member of the SWI/SNF (mating type switching/sucrose nonfermenting) chromatin-remodeling complex, is recently found to be inactivated by promoter hypermethylation in human colorectal cancer. However, the role of this putative tumor suppressor gene in other tumors has not been determined. We evaluated the role of HLTF promoter hypermethylation in gastric cancer. Expression of HLTF was examined by reverse-transcription (RT)-polymerase chain reaction (PCR), and promoter hypermethylation in HLTF was determined by methylation-specific PCR. Bisulfite DNA sequencing was performed to determine the detailed methylation profiles of the promoter region. HLTF expression was lost in two of five gastric cell lines and in 13 (28%) of 46 primary gastric cancers. Accordingly, promoter hypermethylation was detected in the two cell lines and in nine of 13 gastric cancer samples. Of the ten normal gastric specimens and ten paired adjacent nonneoplastic tissues, methylation was detected in only one adjacent nonneoplastic tissue. Bisulfite DNA sequencing of the promoter region of HLTF showed that the CpG island was densely methylated in cell lines and cancer samples; this also appeared to correlate with expression level. Treatment of gastric cell lines that lacked HLTF expression with the demethylating agent 5-azacytidine (5-azaDC) restored HLTF expression. These results suggest that HLTF promoter hypermethylation is frequently demonstrated in human gastric cancer, and inactivation of HLTF or the chromatin-remodeling complex may play a crucial role in gastric carcinogenesis. © 2003 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/en_US
dc.relation.ispartofMolecular Carcinogenesisen_US
dc.subject.meshAdaptor Proteins, Signal Transducingen_US
dc.subject.meshAntimetabolites, Antineoplastic - Pharmacologyen_US
dc.subject.meshAzacitidine - Pharmacologyen_US
dc.subject.meshCarrier Proteinsen_US
dc.subject.meshCpg Islandsen_US
dc.subject.meshDna Methylation - Drug Effectsen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshGastric Mucosa - Cytology - Metabolismen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshHumansen_US
dc.subject.meshNeoplasm Proteins - Genetics - Metabolismen_US
dc.subject.meshNuclear Proteinsen_US
dc.subject.meshPromoter Regions, Genetic - Drug Effects - Physiologyen_US
dc.subject.meshSequence Analysis, Dna - Methodsen_US
dc.subject.meshStomach Neoplasms - Genetics - Metabolismen_US
dc.subject.meshSulfites - Chemistryen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleInactivation of helicase-like transcription factor by promoter hypermethylation in human gastric canceren_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/mc.10124en_US
dc.identifier.pmid12766908-
dc.identifier.scopuseid_2-s2.0-0037533708en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037533708&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume37en_US
dc.identifier.issue2en_US
dc.identifier.spage91en_US
dc.identifier.epage97en_US
dc.identifier.isiWOS:000183315200004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridBai, AHC=7006523130en_US
dc.identifier.scopusauthoridChan, MWY=7402597788en_US
dc.identifier.scopusauthoridChan, KK=8599737700en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridChan, FKL=7202586434en_US
dc.identifier.scopusauthoridNg, EKW=7201647539en_US
dc.identifier.scopusauthoridChung, SCS=19642462800en_US
dc.identifier.scopusauthoridSung, JJY=24473715000en_US

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