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Article: TSLC1 is a tumor suppressor gene associated with metastasis in nasopharyngeal carcinoma

TitleTSLC1 is a tumor suppressor gene associated with metastasis in nasopharyngeal carcinoma
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. 19, p. 9385-9392 How to Cite?
AbstractIn up to 87% of nasopharyngeal carcinoma (NPC) clinical tumor specimens, there was either down-regulation or loss of TSLC1 gene expression. Using a tissue microarray and immunohistochemical staining, the frequency of down-regulated or loss of expression of TSLC1 in metastatic lymph node NPC was 83% and the frequency of loss of expression of TSLC1 was 35%, which was significantly higher than that in primary NPC (12%). To examine the possible growth-suppressive activity of TSLC1 in NPC, three NPC cell lines, HONE1, HNE1, and CNE2, were transfected with the wild-type TSLC1 gene cloned into the pCR3.1 expression vector; a reduction of colony formation ability was observed for all three cell lines. A tetracycline-inducible expression vector, pETE-Bsd, was also used to obtain stable transfectants of TSLC1. There was a dramatic difference between colony formation ability in the presence or absence of doxycycline when the gene is shut off or expressed, respectively, with the tetracycline-inducible system. Tumorigenicity assay results show that the activation of TSLC1 suppresses tumor formation in nude mice and functional inactivation of this gene is observed in all the tumors derived from tumorigenic transfectants. Further studies indicate that expression of TSLC1 inhibits HONE1 cell growth in vitro by arresting cells in G 0-G 1 phase in normal culture conditions, whereas in the absence of serum, TSLC1 induced apoptosis. These findings suggest that TSLC1 is a tumor suppressor gene in NPC, which is significantly associated with lymph node metastases. ©2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/67929
ISSN
2014 Impact Factor: 9.329
2013 SCImago Journal Rankings: 5.627
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLung, HLen_HK
dc.contributor.authorCheung, AKLen_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorKwong, FMen_HK
dc.contributor.authorMurakami, Yen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorSham, JSen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorProtopopov, AIen_HK
dc.contributor.authorZabarovsky, ERen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-09-06T05:59:33Z-
dc.date.available2010-09-06T05:59:33Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Research, 2006, v. 66 n. 19, p. 9385-9392en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67929-
dc.description.abstractIn up to 87% of nasopharyngeal carcinoma (NPC) clinical tumor specimens, there was either down-regulation or loss of TSLC1 gene expression. Using a tissue microarray and immunohistochemical staining, the frequency of down-regulated or loss of expression of TSLC1 in metastatic lymph node NPC was 83% and the frequency of loss of expression of TSLC1 was 35%, which was significantly higher than that in primary NPC (12%). To examine the possible growth-suppressive activity of TSLC1 in NPC, three NPC cell lines, HONE1, HNE1, and CNE2, were transfected with the wild-type TSLC1 gene cloned into the pCR3.1 expression vector; a reduction of colony formation ability was observed for all three cell lines. A tetracycline-inducible expression vector, pETE-Bsd, was also used to obtain stable transfectants of TSLC1. There was a dramatic difference between colony formation ability in the presence or absence of doxycycline when the gene is shut off or expressed, respectively, with the tetracycline-inducible system. Tumorigenicity assay results show that the activation of TSLC1 suppresses tumor formation in nude mice and functional inactivation of this gene is observed in all the tumors derived from tumorigenic transfectants. Further studies indicate that expression of TSLC1 inhibits HONE1 cell growth in vitro by arresting cells in G 0-G 1 phase in normal culture conditions, whereas in the absence of serum, TSLC1 induced apoptosis. These findings suggest that TSLC1 is a tumor suppressor gene in NPC, which is significantly associated with lymph node metastases. ©2006 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://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshCarcinoma, Squamous Cell - genetics - pathology - secondary-
dc.subject.meshGenes, Tumor Suppressor-
dc.subject.meshImmunoglobulins - deficiency - genetics - physiology-
dc.subject.meshLymphatic Metastasis - genetics-
dc.subject.meshMembrane Proteins - deficiency - genetics - physiology-
dc.titleTSLC1 is a tumor suppressor gene associated with metastasis in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=66&issue=19&spage=9385&epage=9392&date=2006&atitle=TSLC1+is+a+tumor+suppressor+gene+associated+with+metastasis+in+nasopharyngeal+carcinomaen_HK
dc.identifier.emailLung, HL: hllung2@hku.hken_HK
dc.identifier.emailCheung, AKL: arthurhk@hku.hken_HK
dc.identifier.emailCheng, Y: yuecheng@hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.emailChua, D: dttchua@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authorityCheung, AKL=rp01769en_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-06-0590en_HK
dc.identifier.pmid17018592-
dc.identifier.scopuseid_2-s2.0-33750331446en_HK
dc.identifier.hkuros173231en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750331446&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue19en_HK
dc.identifier.spage9385en_HK
dc.identifier.epage9392en_HK
dc.identifier.isiWOS:000241014200009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridCheung, AKL=8967932600en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridKwong, FM=8158557800en_HK
dc.identifier.scopusauthoridMurakami, Y=7404145481en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridSham, JS=7101655565en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_HK
dc.identifier.scopusauthoridProtopopov, AI=7006756529en_HK
dc.identifier.scopusauthoridZabarovsky, ER=7007009108en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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