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Article: Functional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinoma
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TitleFunctional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinoma
 
AuthorsLeung Cheung, AK6
Lung, HL6
Hung, SC6
Law, EWL6
Cheng, Y6 5
Yau, WL6
Bangarusamy, DK4
Miller, LD4
Liu, ETB4
Shao, JY2
Kou, CW2
Chua, D3
Zabarovsky, ER1
Tsao, SW3
Stanbridge, EJ7
Lung, ML6
 
KeywordsMolecular Sequence Numbers
 
Issue Date2008
 
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
 
CitationCancer Research, 2008, v. 68 n. 19, p. 8137-8145 [How to Cite?]
DOI: http://dx.doi.org/10.1158/0008-5472.CAN-08-0904
 
AbstractFunctional studies to identify the potential role of a chromosome 3p14-21 gene, protein tyrosine phosphatase receptor type G (PTPRG), were performed. PTPRG was identified as a candidate tumor suppressor gene (TSG) in nasopharyngeal carcinoma (NPC)by differential gene profiling of tumorigenic and nontumorigenic NPC chromosome 3 microcell hybrids (MCH). Down-regulation of this gene was found in tumor segregants when compared with their corresponding tumor-suppressive MCHs, as well as in NPC cell lines and tumor biopsies. Promoter hypermethylation and loss of heterozygosity were found to be important mechanisms contributing to PTPRG silencing. PTPRG overexpression in NPC cell lines induces growth suppression and reduced anchorage-independent growth in vitro. This is the first study to use a tetracycline-responsive vector expression system to study PTPRG stable transfectants. Results indicate its ability to induce significant tumor growth suppression in nude mice under conditions activating transgene expression. These studies now provide functional evidence indicating critical interactions of PTPRG in the extracellular matrix milieu induce cell arrest and changes in cell cycle status. This is associated with inhibition of pRB phosphorylation through down-regulation of cyclin D1. These novel findings enhance our current understanding of how PTPRG may contribute to tumorigenesis. ©2008 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-08-0904
 
ISI Accession Number IDWOS:000260029900053
Funding AgencyGrant Number
People's Republic of ChinaHKUST6112/04M
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Royal Swedish Academy of Sciences
Karohnska Institute
Funding Information:

Grant support: Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of China grant HKUST6112/04M (M.L. Lung), and Swedish Cancer Society, Swedish Research Council, Swedish Institute, Royal Swedish Academy of Sciences, and Karohnska Institute (E.R. Zabarovsky).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLeung Cheung, AK
 
dc.contributor.authorLung, HL
 
dc.contributor.authorHung, SC
 
dc.contributor.authorLaw, EWL
 
dc.contributor.authorCheng, Y
 
dc.contributor.authorYau, WL
 
dc.contributor.authorBangarusamy, DK
 
dc.contributor.authorMiller, LD
 
dc.contributor.authorLiu, ETB
 
dc.contributor.authorShao, JY
 
dc.contributor.authorKou, CW
 
dc.contributor.authorChua, D
 
dc.contributor.authorZabarovsky, ER
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorStanbridge, EJ
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2010-09-17T10:15:47Z
 
dc.date.available2010-09-17T10:15:47Z
 
dc.date.issued2008
 
dc.description.abstractFunctional studies to identify the potential role of a chromosome 3p14-21 gene, protein tyrosine phosphatase receptor type G (PTPRG), were performed. PTPRG was identified as a candidate tumor suppressor gene (TSG) in nasopharyngeal carcinoma (NPC)by differential gene profiling of tumorigenic and nontumorigenic NPC chromosome 3 microcell hybrids (MCH). Down-regulation of this gene was found in tumor segregants when compared with their corresponding tumor-suppressive MCHs, as well as in NPC cell lines and tumor biopsies. Promoter hypermethylation and loss of heterozygosity were found to be important mechanisms contributing to PTPRG silencing. PTPRG overexpression in NPC cell lines induces growth suppression and reduced anchorage-independent growth in vitro. This is the first study to use a tetracycline-responsive vector expression system to study PTPRG stable transfectants. Results indicate its ability to induce significant tumor growth suppression in nude mice under conditions activating transgene expression. These studies now provide functional evidence indicating critical interactions of PTPRG in the extracellular matrix milieu induce cell arrest and changes in cell cycle status. This is associated with inhibition of pRB phosphorylation through down-regulation of cyclin D1. These novel findings enhance our current understanding of how PTPRG may contribute to tumorigenesis. ©2008 American Association for Cancer Research.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationCancer Research, 2008, v. 68 n. 19, p. 8137-8145 [How to Cite?]
DOI: http://dx.doi.org/10.1158/0008-5472.CAN-08-0904
 
dc.identifier.doihttp://dx.doi.org/10.1158/0008-5472.CAN-08-0904
 
dc.identifier.eissn1538-7445
 
dc.identifier.epage8145
 
dc.identifier.hkuros173234
 
dc.identifier.isiWOS:000260029900053
Funding AgencyGrant Number
People's Republic of ChinaHKUST6112/04M
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Royal Swedish Academy of Sciences
Karohnska Institute
Funding Information:

Grant support: Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of China grant HKUST6112/04M (M.L. Lung), and Swedish Cancer Society, Swedish Research Council, Swedish Institute, Royal Swedish Academy of Sciences, and Karohnska Institute (E.R. Zabarovsky).

 
dc.identifier.issn0008-5472
2013 Impact Factor: 9.284
2013 SCImago Journal Rankings: 5.627
 
dc.identifier.issue19
 
dc.identifier.pmid18829573
 
dc.identifier.scopuseid_2-s2.0-54249092901
 
dc.identifier.spage8137
 
dc.identifier.urihttp://hdl.handle.net/10722/91259
 
dc.identifier.volume68
 
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.meshAnimals
 
dc.subject.meshCarcinoma - genetics
 
dc.subject.meshCells, Cultured
 
dc.subject.meshChromosomes, Human, Pair 3
 
dc.subject.meshDNA Methylation
 
dc.subject.meshFemale
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshGenes, Tumor Suppressor - physiology
 
dc.subject.meshGenes, cdc - physiology
 
dc.subject.meshHumans
 
dc.subject.meshLoss of Heterozygosity
 
dc.subject.meshMice
 
dc.subject.meshMice, Inbred BALB C
 
dc.subject.meshMice, Nude
 
dc.subject.meshNasopharyngeal Neoplasms - genetics
 
dc.subject.meshOligonucleotide Array Sequence Analysis
 
dc.subject.meshReceptor-Like Protein Tyrosine Phosphatases, Class 5 - genetics - physiology
 
dc.subjectMolecular Sequence Numbers
 
dc.titleFunctional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinoma
 
dc.typeArticle
 
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Author Affiliations
  1. Karolinska University Hospital
  2. Sun Yat-Sen University Cancer Center
  3. The University of Hong Kong
  4. Genome Institute of Singapore
  5. City of Hope National Med Center
  6. Hong Kong University of Science and Technology
  7. UC Irvine