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Article: TSLC1 is a tumor suppressor gene associated with metastasis in nasopharyngeal carcinoma
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TitleTSLC1 is a tumor suppressor gene associated with metastasis in nasopharyngeal carcinoma
 
AuthorsLung, HL
Cheung, AKL
Xie, D5 3
Cheng, Y4
Kwong, FM
Murakami, Y1
Guan, XY3
Sham, JS3
Chua, D3
Protopopov, AI2
Zabarovsky, ER2
Tsao, SW3
Stanbridge, EJ7
Lung, ML6
 
Issue Date2006
 
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
 
CitationCancer Research, 2006, v. 66 n. 19, p. 9385-9392 [How to Cite?]
DOI: http://dx.doi.org/10.1158/0008-5472.CAN-06-0590
 
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.
 
ISSN0008-5472
2013 Impact Factor: 9.284
2013 SCImago Journal Rankings: 5.627
 
DOIhttp://dx.doi.org/10.1158/0008-5472.CAN-06-0590
 
ISI Accession Number IDWOS:000241014200009
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLung, HL
 
dc.contributor.authorCheung, AKL
 
dc.contributor.authorXie, D
 
dc.contributor.authorCheng, Y
 
dc.contributor.authorKwong, FM
 
dc.contributor.authorMurakami, Y
 
dc.contributor.authorGuan, XY
 
dc.contributor.authorSham, JS
 
dc.contributor.authorChua, D
 
dc.contributor.authorProtopopov, AI
 
dc.contributor.authorZabarovsky, ER
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorStanbridge, EJ
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2010-09-06T05:59:33Z
 
dc.date.available2010-09-06T05:59:33Z
 
dc.date.issued2006
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCancer Research, 2006, v. 66 n. 19, p. 9385-9392 [How to Cite?]
DOI: http://dx.doi.org/10.1158/0008-5472.CAN-06-0590
 
dc.identifier.doihttp://dx.doi.org/10.1158/0008-5472.CAN-06-0590
 
dc.identifier.epage9392
 
dc.identifier.hkuros173231
 
dc.identifier.isiWOS:000241014200009
 
dc.identifier.issn0008-5472
2013 Impact Factor: 9.284
2013 SCImago Journal Rankings: 5.627
 
dc.identifier.issue19
 
dc.identifier.openurl
 
dc.identifier.pmid17018592
 
dc.identifier.scopuseid_2-s2.0-33750331446
 
dc.identifier.spage9385
 
dc.identifier.urihttp://hdl.handle.net/10722/67929
 
dc.identifier.volume66
 
dc.languageeng
 
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofCancer Research
 
dc.relation.referencesReferences in Scopus
 
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 carcinoma
 
dc.typeArticle
 
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Author Affiliations
  1. National Cancer Center Research Institute
  2. Institutionen För Mikrobiologi, Tumör-Och Cellbiologi
  3. The University of Hong Kong
  4. National Naval Medical Center
  5. Sun Yat-Sen University
  6. Hong Kong University of Science and Technology
  7. UC Irvine