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Article: Bmi1 functions as an oncogene independent of Ink4a/Arf repression in hepatic carcinogenesis

TitleBmi1 functions as an oncogene independent of Ink4a/Arf repression in hepatic carcinogenesis
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/
Citation
Molecular Cancer Research, 2009, v. 7 n. 12, p. 1937-1945 How to Cite?
AbstractBmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote hepatic carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development. Copyright © 2009 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/83326
ISSN
2015 Impact Factor: 4.51
2015 SCImago Journal Rankings: 2.534
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
NIHR21CA131625
R01CA136606
R01CA094150
University of California at San Francisco liver centerP30DK026743
Funding Information:

NIH grants R21CA131625 and R01CA136606 (X. Chen), R01CA094150 (G.P. Dimri), and P30DK026743 to the University of California at San Francisco liver center.

References

 

DC FieldValueLanguage
dc.contributor.authorXu, CRen_HK
dc.contributor.authorLee, Sen_HK
dc.contributor.authorHo, Cen_HK
dc.contributor.authorBommi, Pen_HK
dc.contributor.authorHuang, SAen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorDimri, GPen_HK
dc.contributor.authorChen, Xen_HK
dc.date.accessioned2010-09-06T08:39:42Z-
dc.date.available2010-09-06T08:39:42Z-
dc.date.issued2009en_HK
dc.identifier.citationMolecular Cancer Research, 2009, v. 7 n. 12, p. 1937-1945en_HK
dc.identifier.issn1541-7786en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83326-
dc.description.abstractBmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote hepatic carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development. Copyright © 2009 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/en_HK
dc.relation.ispartofMolecular Cancer Researchen_HK
dc.subject.meshCarcinoma, Hepatocellular - genetics - metabolism - pathology-
dc.subject.meshLiver Neoplasms - genetics - metabolism - pathology-
dc.subject.meshNuclear Proteins - genetics - metabolism-
dc.subject.meshProto-Oncogene Proteins - genetics - metabolism-
dc.subject.meshRepressor Proteins - genetics - metabolism-
dc.titleBmi1 functions as an oncogene independent of Ink4a/Arf repression in hepatic carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1541-7786&volume=7&issue=12&spage=1937&epage=1945&date=2009&atitle=Bmi1+functions+as+an+oncogene+independent+of+Ink4A/Arf+repression+in+hepatic+carcinogenesisen_HK
dc.identifier.emailCheung, ST: stcheung@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ST=rp00457en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1541-7786.MCR-09-0333en_HK
dc.identifier.pmid19934271-
dc.identifier.pmcidPMC2796287-
dc.identifier.scopuseid_2-s2.0-73849147288en_HK
dc.identifier.hkuros168604en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-73849147288&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1937en_HK
dc.identifier.epage1945en_HK
dc.identifier.isiWOS:000272965600005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, CR=25959422300en_HK
dc.identifier.scopusauthoridLee, S=7601410760en_HK
dc.identifier.scopusauthoridHo, C=8914892800en_HK
dc.identifier.scopusauthoridBommi, P=22956780800en_HK
dc.identifier.scopusauthoridHuang, SA=7405422564en_HK
dc.identifier.scopusauthoridCheung, ST=7202473497en_HK
dc.identifier.scopusauthoridDimri, GP=6701892352en_HK
dc.identifier.scopusauthoridChen, X=14618971500en_HK

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