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Article: Anti-apoptotic role of BARF1 in gastric cancer cells

TitleAnti-apoptotic role of BARF1 in gastric cancer cells
Authors
KeywordsApoptosis
BARF1
EBV
Gastric cancer
Issue Date2006
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2006, v. 238 n. 1, p. 90-103 How to Cite?
AbstractEpstein-Barr virus (EBV) infection has been implicated in the carcinogenesis of several types of human cancer, including gastric cancer. In contrast to two other EBV-related malingancies, nasopharyngeal carcinoma and Hodgkins Lympomain which the latent membrane protein (LMP)-1 is often detected, in gastric cancer, BARF1, one of the early EBV genes, is frequently expressed in EBV-positive specimens. This indicates that expression of BARF1 may play a positive role in the development of gastric cancer. The aim of this study was to investigate the effect of BARF1 expression in gastric cancer cells. First, a retroviral vector containing the full length BARF1 gene was transfected into an EBV negative gastric cancer cell line, BGC823, and stable transfectants expressing ectopic BARF1 were generated. Microarray analysis was then performed and gene expression profiles were analysed and compared between the cells expressing ectopic BARF1 and the vector control. In addition, the effect of BARF1 on gastric cancer cell proliferation and apoptosis was investigated by MTT assay, DAPI staining, flow cytometry as well as Western blotting. We found that expression of BARF1 in gastric cancer cells led to significant alterations of gene expression, especially genes related to proliferation and apoptosis. In addition, the BARF1 expressing cells were more resistant to apoptosis induced by a commonly used anticancer drug, taxol. This chemo-protective effect of BARF1 was associated with increased Bcl-2 and Bax ratio and decreased expression of cleaved PARP, but not alterations in cell proliferation. Our results suggest that BARF1 expression in gastric cancer cells may provide a protective role against apoptosis through an increased Bcl-2 to Bax ratio, thus promoting cancer cell survival. © 2005 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67715
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Qen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorOoka, Ten_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorFu, Sen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:57:36Z-
dc.date.available2010-09-06T05:57:36Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Letters, 2006, v. 238 n. 1, p. 90-103en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67715-
dc.description.abstractEpstein-Barr virus (EBV) infection has been implicated in the carcinogenesis of several types of human cancer, including gastric cancer. In contrast to two other EBV-related malingancies, nasopharyngeal carcinoma and Hodgkins Lympomain which the latent membrane protein (LMP)-1 is often detected, in gastric cancer, BARF1, one of the early EBV genes, is frequently expressed in EBV-positive specimens. This indicates that expression of BARF1 may play a positive role in the development of gastric cancer. The aim of this study was to investigate the effect of BARF1 expression in gastric cancer cells. First, a retroviral vector containing the full length BARF1 gene was transfected into an EBV negative gastric cancer cell line, BGC823, and stable transfectants expressing ectopic BARF1 were generated. Microarray analysis was then performed and gene expression profiles were analysed and compared between the cells expressing ectopic BARF1 and the vector control. In addition, the effect of BARF1 on gastric cancer cell proliferation and apoptosis was investigated by MTT assay, DAPI staining, flow cytometry as well as Western blotting. We found that expression of BARF1 in gastric cancer cells led to significant alterations of gene expression, especially genes related to proliferation and apoptosis. In addition, the BARF1 expressing cells were more resistant to apoptosis induced by a commonly used anticancer drug, taxol. This chemo-protective effect of BARF1 was associated with increased Bcl-2 and Bax ratio and decreased expression of cleaved PARP, but not alterations in cell proliferation. Our results suggest that BARF1 expression in gastric cancer cells may provide a protective role against apoptosis through an increased Bcl-2 to Bax ratio, thus promoting cancer cell survival. © 2005 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectApoptosisen_HK
dc.subjectBARF1en_HK
dc.subjectEBVen_HK
dc.subjectGastric canceren_HK
dc.subject.meshAntineoplastic Agents, Phytogenic - pharmacologyen_HK
dc.subject.meshApoptosis - drug effects - geneticsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - drug effects - geneticsen_HK
dc.subject.meshGene Transfer Techniquesen_HK
dc.subject.meshGenetic Vectors - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshOligonucleotide Array Sequence Analysisen_HK
dc.subject.meshPaclitaxel - pharmacologyen_HK
dc.subject.meshStomach Neoplasms - drug therapy - genetics - metabolismen_HK
dc.subject.meshViral Proteins - genetics - pharmacology - physiologyen_HK
dc.titleAnti-apoptotic role of BARF1 in gastric cancer cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=xx&spage=1&epage=14&date=2005&atitle=Anti-apoptotic+role+of+BARF1+in+gastric+cancer+cellsen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2005.06.023en_HK
dc.identifier.pmid16054293-
dc.identifier.scopuseid_2-s2.0-33745028169en_HK
dc.identifier.hkuros108861en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745028169&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume238en_HK
dc.identifier.issue1en_HK
dc.identifier.spage90en_HK
dc.identifier.epage103en_HK
dc.identifier.isiWOS:000238931400010-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridWang, Q=7406910452en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridOoka, T=7004710044en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridCheung, HW=7201839381en_HK
dc.identifier.scopusauthoridFu, S=7402732420en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK

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