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Article: Interaction of deleted in liver cancer 1 with Tensin2 in caveolae and implications in tumor suppression

TitleInteraction of deleted in liver cancer 1 with Tensin2 in caveolae and implications in tumor suppression
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2006, v. 66 n. 17, p. 8367-8372 How to Cite?
AbstractDeleted in liver cancer 1 (DLC1) is a recently identified tumor suppressor gene frequently underexpressed in hepatocellular carcinoma (HCC). DLC1 encodes a Rho GTPase-activating protein domain that exhibits growth-suppressive activity in HCC cell lines. Our recent finding has revealed that inhibition of Rho-mediated actin stress fiber formation by DLC1 is associated with its growth inhibitory activity. In the present study, we identified tensin2 as the novel binding partner of DLC1. Tensin2 belongs to a new family of focal adhesion proteins that play key roles in cytoskeleton organization and signal transduction. Dysregulation of tensin proteins has previously been implicated in human cancers. Tensin2 is highly expressed in human liver. Introduction of tensin2 into HCC cell lines with low expression of tensin2 caused significant growth inhibition and induction of apoptosis. Tensin2 directly interacted with DLC1 in vitro and in vivo. Both proteins localized to punctate structures in the cytoplasm. Sequence analysis of DLC1 and tensin2 identified caveolin-1 binding motif in both proteins. In vivo immunoprecipitation study confirmed that both proteins indeed interacted with endogenous caveolin-1, which is the major structural component of caveolae. Our findings presented here suggest a new model for the action of DLC1 in hepatocytes, whereby DLC1-tensin2 complex interacts with Rho GTPases in caveolae to effect cytoskeletal reorganization. ©2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/147548
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, JWPen_US
dc.contributor.authorKo, FCFen_US
dc.contributor.authorChan, CYen_US
dc.contributor.authorJin, DYen_US
dc.contributor.authorNg, IOLen_US
dc.date.accessioned2012-05-29T06:04:31Z-
dc.date.available2012-05-29T06:04:31Z-
dc.date.issued2006en_US
dc.identifier.citationCancer Research, 2006, v. 66 n. 17, p. 8367-8372en_US
dc.identifier.issn0008-5472en_US
dc.identifier.urihttp://hdl.handle.net/10722/147548-
dc.description.abstractDeleted in liver cancer 1 (DLC1) is a recently identified tumor suppressor gene frequently underexpressed in hepatocellular carcinoma (HCC). DLC1 encodes a Rho GTPase-activating protein domain that exhibits growth-suppressive activity in HCC cell lines. Our recent finding has revealed that inhibition of Rho-mediated actin stress fiber formation by DLC1 is associated with its growth inhibitory activity. In the present study, we identified tensin2 as the novel binding partner of DLC1. Tensin2 belongs to a new family of focal adhesion proteins that play key roles in cytoskeleton organization and signal transduction. Dysregulation of tensin proteins has previously been implicated in human cancers. Tensin2 is highly expressed in human liver. Introduction of tensin2 into HCC cell lines with low expression of tensin2 caused significant growth inhibition and induction of apoptosis. Tensin2 directly interacted with DLC1 in vitro and in vivo. Both proteins localized to punctate structures in the cytoplasm. Sequence analysis of DLC1 and tensin2 identified caveolin-1 binding motif in both proteins. In vivo immunoprecipitation study confirmed that both proteins indeed interacted with endogenous caveolin-1, which is the major structural component of caveolae. Our findings presented here suggest a new model for the action of DLC1 in hepatocytes, whereby DLC1-tensin2 complex interacts with Rho GTPases in caveolae to effect cytoskeletal reorganization. ©2006 American Association for Cancer Research.en_US
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_US
dc.relation.ispartofCancer Researchen_US
dc.subject.meshBinding Sitesen_US
dc.subject.meshCarcinoma, Hepatocellular - Genetics - Metabolismen_US
dc.subject.meshCaveolae - Pathology - Physiologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshColony-Forming Units Assayen_US
dc.subject.meshGtpase-Activating Proteins - Metabolismen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGenes, Reporteren_US
dc.subject.meshGlutathione Transferase - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshKidneyen_US
dc.subject.meshLiver - Physiologyen_US
dc.subject.meshLiver Neoplasms - Genetics - Metabolismen_US
dc.subject.meshMicrofilament Proteins - Genetics - Metabolismen_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshPhosphoric Monoester Hydrolases - Genetics - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTumor Suppressor Proteins - Genetics - Metabolismen_US
dc.titleInteraction of deleted in liver cancer 1 with Tensin2 in caveolae and implications in tumor suppressionen_US
dc.typeArticleen_US
dc.identifier.emailYam, JWP:judyyam@pathology.hku.hken_US
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_US
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_US
dc.identifier.authorityYam, JWP=rp00468en_US
dc.identifier.authorityJin, DY=rp00452en_US
dc.identifier.authorityNg, IOL=rp00335en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-05-2850en_US
dc.identifier.pmid16951145en_US
dc.identifier.scopuseid_2-s2.0-33748994597en_US
dc.identifier.hkuros128647-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33748994597&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume66en_US
dc.identifier.issue17en_US
dc.identifier.spage8367en_US
dc.identifier.epage8372en_US
dc.identifier.isiWOS:000240329400010-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYam, JWP=6603711123en_US
dc.identifier.scopusauthoridKo, FCF=14630572500en_US
dc.identifier.scopusauthoridChan, CY=8277448300en_US
dc.identifier.scopusauthoridJin, DY=7201973614en_US
dc.identifier.scopusauthoridNg, IOL=7102753722en_US

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