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Article: Deleted in liver cancer 2 (DLC2) was dispensable for development and its deficiency did not aggravate hepatocarcinogenesis

TitleDeleted in liver cancer 2 (DLC2) was dispensable for development and its deficiency did not aggravate hepatocarcinogenesis
Authors
Issue Date2009
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2009, v. 4 n. 8, article no. e6566 How to Cite?
AbstractDLC2 (deleted in liver cancer 2), a Rho GTPase-activating protein, was previously shown to be underexpressed in human hepatocellular carcinoma and has tumor suppressor functions in cell culture models. We generated DLC2-deficient mice to investigate the tumor suppressor role of DLC2 in hepatocarcinogenesis and the function of DLC2 in vivo. In this study, we found that, unlike homologous DLC1, which is essential for embryonic development, DLC2 was dispensable for embryonic development and DLC2-deficient mice could survive to adulthood. We also did not observe a higher incidence of liver tumor formation or diethylnitrosamine (DEN)-induced hepatocarcinogenesis in DLC2-deficient mice. However, we observed that DLC2-deficient mice were smaller and had less adipose tissue than the wild type mice. These phenotypes were not due to reduction of cell size or defect in adipogenesis, as observed in the 190B RhoGAP-deficient mouse model. Together, these results suggest that deficiency in DLC2 alone does not enhance hepatocarcinogenesis. © 2009 Yau et al.
Persistent Identifierhttp://hdl.handle.net/10722/67503
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYau, TOen_HK
dc.contributor.authorLeung, THYen_HK
dc.contributor.authorLam, Sen_HK
dc.contributor.authorCheung, OFen_HK
dc.contributor.authorTung, EKKen_HK
dc.contributor.authorKhong, PLen_HK
dc.contributor.authorLam, Aen_HK
dc.contributor.authorChung, Sen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-06T05:55:42Z-
dc.date.available2010-09-06T05:55:42Z-
dc.date.issued2009en_HK
dc.identifier.citationPlos One, 2009, v. 4 n. 8, article no. e6566en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67503-
dc.description.abstractDLC2 (deleted in liver cancer 2), a Rho GTPase-activating protein, was previously shown to be underexpressed in human hepatocellular carcinoma and has tumor suppressor functions in cell culture models. We generated DLC2-deficient mice to investigate the tumor suppressor role of DLC2 in hepatocarcinogenesis and the function of DLC2 in vivo. In this study, we found that, unlike homologous DLC1, which is essential for embryonic development, DLC2 was dispensable for embryonic development and DLC2-deficient mice could survive to adulthood. We also did not observe a higher incidence of liver tumor formation or diethylnitrosamine (DEN)-induced hepatocarcinogenesis in DLC2-deficient mice. However, we observed that DLC2-deficient mice were smaller and had less adipose tissue than the wild type mice. These phenotypes were not due to reduction of cell size or defect in adipogenesis, as observed in the 190B RhoGAP-deficient mouse model. Together, these results suggest that deficiency in DLC2 alone does not enhance hepatocarcinogenesis. © 2009 Yau et al.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsP L o S One. Copyright © Public Library of Science.en_HK
dc.subject.meshAdipose Tissue - physiology-
dc.subject.meshAnimals-
dc.subject.meshBase Sequence-
dc.subject.meshLiver Neoplasms, Experimental - chemically induced - physiopathology-
dc.subject.meshTumor Suppressor Proteins - genetics - physiology-
dc.titleDeleted in liver cancer 2 (DLC2) was dispensable for development and its deficiency did not aggravate hepatocarcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=4&issue=8&spage=e6566&epage=&date=2009&atitle=Deleted+in+liver+cancer+2+(DLC2)+was+dispensable+for+development+and+its+deficiency+did+not+aggravate+hepatocarcinogenesisen_HK
dc.identifier.emailKhong, PL:plkhong@hkucc.hku.hken_HK
dc.identifier.emailChung, S:skchung@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityKhong, PL=rp00467en_HK
dc.identifier.authorityChung, S=rp00381en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0006566en_HK
dc.identifier.pmid19440389-
dc.identifier.pmid19668331-
dc.identifier.pmcidPMC2718616-
dc.identifier.scopuseid_2-s2.0-68749114021en_HK
dc.identifier.hkuros166583en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68749114021&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue8en_HK
dc.identifier.spagee6566-
dc.identifier.spagearticle no. e6566-
dc.identifier.epagee6566-
dc.identifier.epagearticle no. e6566-
dc.identifier.isiWOS:000268773300008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYau, TO=7006540669en_HK
dc.identifier.scopusauthoridLeung, THY=7202110922en_HK
dc.identifier.scopusauthoridLam, S=35077630000en_HK
dc.identifier.scopusauthoridCheung, OF=16311432900en_HK
dc.identifier.scopusauthoridTung, EKK=7003519614en_HK
dc.identifier.scopusauthoridKhong, PL=7006693233en_HK
dc.identifier.scopusauthoridLam, A=7201848036en_HK
dc.identifier.scopusauthoridChung, S=7404292976en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

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