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Article: Tensin2 variant 3 is associated with aggressive tumor behavior in human hepatocellular carcinoma

TitleTensin2 variant 3 is associated with aggressive tumor behavior in human hepatocellular carcinoma
Authors
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2006, v. 44 n. 4, p. 881-890 How to Cite?
AbstractTensins are a new family of proteins that act as an important link among extracellular matrix, actin cytoskeleton, and signal transduction and have been implicated in human cancers. Tensin2 was initially identified in a search for new tensin family members that share extensive sequence homology with tensin1. Tensin2 was highly expressed in liver tissues. A recent study reported that one of the splicing variants of tensin2, variant 3, promotes cell migration. In the present study, we aimed to elucidate the role of variant 3 in hepatocarcinogenesis by assessing the expression of variant 3 mRNA in hepatocellular carcinoma (HCC) tissue and ectopically expressing variant 3 in HCC cell lines. Analysis of variant 3 expression in human HCC tissue revealed it was overexpressed in 46% (23/50) of tumor tissues as compared with the corresponding nontumorous livers. High expression of variant 3 was significantly associated with venous invasion (P = .037), tumor microsatellite formation (P = .022), and tumor nonencapsulation (P = .049). Our ectopic expression study showed that variant 3 significantly promoted the cell growth and motility of HCC cells. The clonal transfectants of variant 3 were more closely packed and resulted in a higher saturation density than in the control vector transfectants. Variant 3 expression also enhanced the proliferation rate in culture and in vivo tumorigenicity in nude mice. In conclusion, we reveal a novel role for variant 3 in the progression of HCC and suggest the feasibility of elevated variant 3 expression as a tumor progression marker for HCC. Copyright © 2006 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/68162
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, JWPen_HK
dc.contributor.authorKo, FCFen_HK
dc.contributor.authorChan, CYen_HK
dc.contributor.authorYau, TOen_HK
dc.contributor.authorTung, EKKen_HK
dc.contributor.authorLeung, THYen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2010-09-06T06:01:57Z-
dc.date.available2010-09-06T06:01:57Z-
dc.date.issued2006en_HK
dc.identifier.citationHepatology, 2006, v. 44 n. 4, p. 881-890en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68162-
dc.description.abstractTensins are a new family of proteins that act as an important link among extracellular matrix, actin cytoskeleton, and signal transduction and have been implicated in human cancers. Tensin2 was initially identified in a search for new tensin family members that share extensive sequence homology with tensin1. Tensin2 was highly expressed in liver tissues. A recent study reported that one of the splicing variants of tensin2, variant 3, promotes cell migration. In the present study, we aimed to elucidate the role of variant 3 in hepatocarcinogenesis by assessing the expression of variant 3 mRNA in hepatocellular carcinoma (HCC) tissue and ectopically expressing variant 3 in HCC cell lines. Analysis of variant 3 expression in human HCC tissue revealed it was overexpressed in 46% (23/50) of tumor tissues as compared with the corresponding nontumorous livers. High expression of variant 3 was significantly associated with venous invasion (P = .037), tumor microsatellite formation (P = .022), and tumor nonencapsulation (P = .049). Our ectopic expression study showed that variant 3 significantly promoted the cell growth and motility of HCC cells. The clonal transfectants of variant 3 were more closely packed and resulted in a higher saturation density than in the control vector transfectants. Variant 3 expression also enhanced the proliferation rate in culture and in vivo tumorigenicity in nude mice. In conclusion, we reveal a novel role for variant 3 in the progression of HCC and suggest the feasibility of elevated variant 3 expression as a tumor progression marker for HCC. Copyright © 2006 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCarcinoma, Hepatocellular - pathologyen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Movement - physiologyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Neoplasms - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMicrofilament Proteins - genetics - metabolismen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshPhosphoprotein Phosphatases - metabolismen_HK
dc.subject.meshPhosphoric Monoester Hydrolases - genetics - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Markers, Biological - genetics - metabolismen_HK
dc.titleTensin2 variant 3 is associated with aggressive tumor behavior in human hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=44&spage=881&epage=890&date=2006&atitle=Tensin2+variant+3+is+associated+with+aggressive+tumor+behavior+in+human+hepatocellular+carcinomaen_HK
dc.identifier.emailYam, JWP:judyyam@pathology.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityYam, JWP=rp00468en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.21339en_HK
dc.identifier.pmid17006924-
dc.identifier.scopuseid_2-s2.0-33750631858en_HK
dc.identifier.hkuros128651en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750631858&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue4en_HK
dc.identifier.spage881en_HK
dc.identifier.epage890en_HK
dc.identifier.eissn1527-3350-
dc.identifier.isiWOS:000241338200014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYam, JWP=6603711123en_HK
dc.identifier.scopusauthoridKo, FCF=14630572500en_HK
dc.identifier.scopusauthoridChan, CY=8277448300en_HK
dc.identifier.scopusauthoridYau, TO=7006540669en_HK
dc.identifier.scopusauthoridTung, EKK=7003519614en_HK
dc.identifier.scopusauthoridLeung, THY=7202110922en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

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