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Article: BRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinoma

TitleBRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinoma
Authors
KeywordsAntiapoptosis
BRE
BRE-specific monoclonal antibody
Fas-mediated acute liver failure
Human hepatocellular carcinoma
Tumorigenesis
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2008, v. 27 n. 9, p. 1208-1217 How to Cite?
AbstractBRE binds to the cytoplasmic domains of tumor necrosis factor receptor-1 and Fas, and in cell lines can attenuate death receptor-initiated apoptosis by inhibiting t-BID-induced activation of the mitochondrial apoptotic pathway. Overexpression of BRE by transfection can also attenuate intrinsic apoptosis and promote growth of the transfected Lewis lung carcinoma line in mice. There is, however, a complete lack of in vivo data about the protein. Here, we report that by using our BRE-specific monoclonal antibody on the immunohistochemistry of 123 specimens of human hepatocellular carcinoma (HCC), significant differences in BRE expression levels between the paired tumoral and non-tumoral regions (P<2.2e-16) were found. Marked overexpression of BRE was detected in majority of the tumors, whereas most non-tumoral regions expressed the same low level of the protein as in normal livers. To investigate whether BRE overexpression could promote cell survival in vivo, liver-specific transgenic BRE mice were generated and found to be significantly resistant to Fas-mediated lethal hepatic apoptosis. The transgenic model also revealed post-transcriptional regulation of Bre level in the liver, which was not observed in HCC and non-HCC cell lines. Indeed, all cell lines analysed express high levels of BRE. In conclusion, BRE is antiapoptotic in vivo, and may promote tumorigenesis when overexpressed. © 2008 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77547
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, BCLen_HK
dc.contributor.authorChing, AKKen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChen, Sen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorLai, PBSen_HK
dc.contributor.authorTang, NLSen_HK
dc.contributor.authorShaw, PCen_HK
dc.contributor.authorChan, JYHen_HK
dc.contributor.authorJames, AEen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLim, PLen_HK
dc.contributor.authorLee, KKHen_HK
dc.contributor.authorChui, YLen_HK
dc.date.accessioned2010-09-06T07:33:05Z-
dc.date.available2010-09-06T07:33:05Z-
dc.date.issued2008en_HK
dc.identifier.citationOncogene, 2008, v. 27 n. 9, p. 1208-1217en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77547-
dc.description.abstractBRE binds to the cytoplasmic domains of tumor necrosis factor receptor-1 and Fas, and in cell lines can attenuate death receptor-initiated apoptosis by inhibiting t-BID-induced activation of the mitochondrial apoptotic pathway. Overexpression of BRE by transfection can also attenuate intrinsic apoptosis and promote growth of the transfected Lewis lung carcinoma line in mice. There is, however, a complete lack of in vivo data about the protein. Here, we report that by using our BRE-specific monoclonal antibody on the immunohistochemistry of 123 specimens of human hepatocellular carcinoma (HCC), significant differences in BRE expression levels between the paired tumoral and non-tumoral regions (P<2.2e-16) were found. Marked overexpression of BRE was detected in majority of the tumors, whereas most non-tumoral regions expressed the same low level of the protein as in normal livers. To investigate whether BRE overexpression could promote cell survival in vivo, liver-specific transgenic BRE mice were generated and found to be significantly resistant to Fas-mediated lethal hepatic apoptosis. The transgenic model also revealed post-transcriptional regulation of Bre level in the liver, which was not observed in HCC and non-HCC cell lines. Indeed, all cell lines analysed express high levels of BRE. In conclusion, BRE is antiapoptotic in vivo, and may promote tumorigenesis when overexpressed. © 2008 Nature Publishing Group All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectAntiapoptosisen_HK
dc.subjectBREen_HK
dc.subjectBRE-specific monoclonal antibodyen_HK
dc.subjectFas-mediated acute liver failureen_HK
dc.subjectHuman hepatocellular carcinomaen_HK
dc.subjectTumorigenesisen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntibodies, Monoclonal - pharmacologyen_HK
dc.subject.meshAntibody Specificityen_HK
dc.subject.meshApoptosis - geneticsen_HK
dc.subject.meshApoptosis Regulatory Proteins - biosynthesis - genetics - physiologyen_HK
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshHeLa Cellsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshJurkat Cellsen_HK
dc.subject.meshLiver Neoplasms - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred ICRen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshNerve Tissue Proteins - biosynthesis - genetics - immunology - physiologyen_HK
dc.titleBRE is an antiapoptotic protein in vivo and overexpressed in human hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=27&spage=1208&epage=17&date=2007&atitle=BRE+is+an+antiapoptotic+protein+in+vivo+and+overexpressed+in+human+hepatocellular+carcinomaen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.onc.1210733en_HK
dc.identifier.pmid17704801-
dc.identifier.scopuseid_2-s2.0-39749096628en_HK
dc.identifier.hkuros149240en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39749096628&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1208en_HK
dc.identifier.epage1217en_HK
dc.identifier.isiWOS:000253407000003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, BCL=7201530794en_HK
dc.identifier.scopusauthoridChing, AKK=35083263600en_HK
dc.identifier.scopusauthoridTo, KF=36785812800en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChen, S=35083162200en_HK
dc.identifier.scopusauthoridLi, Q=36067406200en_HK
dc.identifier.scopusauthoridLai, PBS=7202946421en_HK
dc.identifier.scopusauthoridTang, NLS=55357657900en_HK
dc.identifier.scopusauthoridShaw, PC=35599523600en_HK
dc.identifier.scopusauthoridChan, JYH=27168376500en_HK
dc.identifier.scopusauthoridJames, AE=7402663799en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLim, PL=7202592401en_HK
dc.identifier.scopusauthoridLee, KKH=8518575700en_HK
dc.identifier.scopusauthoridChui, YL=7004982375en_HK
dc.identifier.citeulike1577897-

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