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Article: Lentivirus-mediated RNA interference targeting enhancer of zeste homolog 2 inhibits hepatocellular carcinoma growth through down-regulation of stathmin

TitleLentivirus-mediated RNA interference targeting enhancer of zeste homolog 2 inhibits hepatocellular carcinoma growth through down-regulation of stathmin
Authors
Issue Date2007
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2007, v. 46 n. 1, p. 200-208 How to Cite?
AbstractEnhancer of zeste homolog 2 (EZH2) has been shown to be overexpressed in hepatocellular (HCC). We investigated the potential role of EZH2 in HCC tumorigenesis and examined the usefulness of RNA interference (RNAi) targeting EZH2 as a form of HCC treatment. Lentivirus-mediated RNAi was employed to knock-down EZH2 expression in human hepatoma cells to study the function of EZH2 in tumorigenesis and evaluate the treatment efficacy. Lentivirus-mediated RNAi effectively reduced EZH2 expression. Suppression of EZH2 in HCC cells significandy reduced their growth rate in vitro and markedly diminished their tumorigenicity in vivo. Moreover, in a mice model of established large-sized HCC, we showed that intratumor injection of lentiviral (Lenti)-shRNA (short hairpin RNA) or siRNA (small interfering RNA) targeting EZH2 produced significant tumor regression. To understand its molecular mechanism of action, we employed proteomic profiling technique and found that stathmin 1 is the downstream target of EZH2, as Lenti-shEZH2 treatment decreased stathmin protein expression, and ectopic overexpression of stathmin prevented Lenti-shEZH2 mediated tumor growth inhibition. Conclusion: Results from our study suggested for the first time that EZH2 plays a key role in HCC tumorigenesis, and is a novel therapeutic target for HCC. Copyright © 2007 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/168130
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_US
dc.contributor.authorLin, MCen_US
dc.contributor.authorYao, Hen_US
dc.contributor.authorWang, Hen_US
dc.contributor.authorZhang, AQen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorHui, CKen_US
dc.contributor.authorLau, GKen_US
dc.contributor.authorHe, MLen_US
dc.contributor.authorSung, Jen_US
dc.contributor.authorKung, HFen_US
dc.date.accessioned2012-10-08T03:15:28Z-
dc.date.available2012-10-08T03:15:28Z-
dc.date.issued2007en_US
dc.identifier.citationHepatology, 2007, v. 46 n. 1, p. 200-208en_US
dc.identifier.issn0270-9139en_US
dc.identifier.urihttp://hdl.handle.net/10722/168130-
dc.description.abstractEnhancer of zeste homolog 2 (EZH2) has been shown to be overexpressed in hepatocellular (HCC). We investigated the potential role of EZH2 in HCC tumorigenesis and examined the usefulness of RNA interference (RNAi) targeting EZH2 as a form of HCC treatment. Lentivirus-mediated RNAi was employed to knock-down EZH2 expression in human hepatoma cells to study the function of EZH2 in tumorigenesis and evaluate the treatment efficacy. Lentivirus-mediated RNAi effectively reduced EZH2 expression. Suppression of EZH2 in HCC cells significandy reduced their growth rate in vitro and markedly diminished their tumorigenicity in vivo. Moreover, in a mice model of established large-sized HCC, we showed that intratumor injection of lentiviral (Lenti)-shRNA (short hairpin RNA) or siRNA (small interfering RNA) targeting EZH2 produced significant tumor regression. To understand its molecular mechanism of action, we employed proteomic profiling technique and found that stathmin 1 is the downstream target of EZH2, as Lenti-shEZH2 treatment decreased stathmin protein expression, and ectopic overexpression of stathmin prevented Lenti-shEZH2 mediated tumor growth inhibition. Conclusion: Results from our study suggested for the first time that EZH2 plays a key role in HCC tumorigenesis, and is a novel therapeutic target for HCC. Copyright © 2007 by the American Association for the Study of Liver Diseases.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_US
dc.relation.ispartofHepatologyen_US
dc.subject.meshCarcinoma, Hepatocellular - Pathologyen_US
dc.subject.meshCell Culture Techniquesen_US
dc.subject.meshCell Division - Geneticsen_US
dc.subject.meshCloning, Molecularen_US
dc.subject.meshDna-Binding Proteins - Geneticsen_US
dc.subject.meshEnhancer Elements, Geneticen_US
dc.subject.meshGene Expression Regulation, Viralen_US
dc.subject.meshHumansen_US
dc.subject.meshLentivirus - Geneticsen_US
dc.subject.meshLiver - Pathology - Physiologyen_US
dc.subject.meshLiver Neoplasms - Pathologyen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshRna Interference - Physiologyen_US
dc.subject.meshRna, Viral - Geneticsen_US
dc.subject.meshRestriction Mappingen_US
dc.subject.meshStathmin - Geneticsen_US
dc.subject.meshTranscription Factors - Geneticsen_US
dc.titleLentivirus-mediated RNA interference targeting enhancer of zeste homolog 2 inhibits hepatocellular carcinoma growth through down-regulation of stathminen_US
dc.typeArticleen_US
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MC=rp00746en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1002/hep.21668en_US
dc.identifier.pmid17596871-
dc.identifier.scopuseid_2-s2.0-34547487035en_US
dc.identifier.hkuros129166-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34547487035&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume46en_US
dc.identifier.issue1en_US
dc.identifier.spage200en_US
dc.identifier.epage208en_US
dc.identifier.isiWOS:000247637000026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChen, Y=24075600300en_US
dc.identifier.scopusauthoridLin, MC=7404816359en_US
dc.identifier.scopusauthoridYao, H=13104506400en_US
dc.identifier.scopusauthoridWang, H=8443997400en_US
dc.identifier.scopusauthoridZhang, AQ=8883727100en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridHui, CK=7202876933en_US
dc.identifier.scopusauthoridLau, GK=7102301257en_US
dc.identifier.scopusauthoridHe, ML=35080389700en_US
dc.identifier.scopusauthoridSung, J=35405352400en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US
dc.identifier.citeulike2235175-

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