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Article: Functional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinoma

TitleFunctional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinoma
Authors
KeywordsMolecular Sequence Numbers
Issue Date2008
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2008, v. 68 n. 19, p. 8137-8145 How to Cite?
Abstract
Functional 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.
Persistent Identifierhttp://hdl.handle.net/10722/91259
ISSN
2013 Impact Factor: 9.284
2013 SCImago Journal Rankings: 5.627
ISI Accession Number ID
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).

References

 

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
DC FieldValueLanguage
dc.contributor.authorLeung Cheung, AKen_HK
dc.contributor.authorLung, HLen_HK
dc.contributor.authorHung, SCen_HK
dc.contributor.authorLaw, EWLen_HK
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorYau, WLen_HK
dc.contributor.authorBangarusamy, DKen_HK
dc.contributor.authorMiller, LDen_HK
dc.contributor.authorLiu, ETBen_HK
dc.contributor.authorShao, JYen_HK
dc.contributor.authorKou, CWen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorZabarovsky, ERen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-09-17T10:15:47Z-
dc.date.available2010-09-17T10:15:47Z-
dc.date.issued2008en_HK
dc.identifier.citationCancer Research, 2008, v. 68 n. 19, p. 8137-8145en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91259-
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.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.subjectMolecular Sequence Numbersen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCarcinoma - geneticsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshChromosomes, Human, Pair 3en_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGenes, Tumor Suppressor - physiologyen_HK
dc.subject.meshGenes, cdc - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNasopharyngeal Neoplasms - geneticsen_HK
dc.subject.meshOligonucleotide Array Sequence Analysisen_HK
dc.subject.meshReceptor-Like Protein Tyrosine Phosphatases, Class 5 - genetics - physiologyen_HK
dc.titleFunctional analysis of a cell cycle-associated, tumor-suppressive gene, protein tyrosine phosphatase receptor type G, in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung Cheung, AK: arthurhk@hku.hken_HK
dc.identifier.emailLung, HL: hllung2@hku.hken_HK
dc.identifier.emailCheng, Y: yuecheng@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.authorityLeung Cheung, AK=rp01769en_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-08-0904en_HK
dc.identifier.pmid18829573en_HK
dc.identifier.scopuseid_2-s2.0-54249092901en_HK
dc.identifier.hkuros173234-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54249092901&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume68en_HK
dc.identifier.issue19en_HK
dc.identifier.spage8137en_HK
dc.identifier.epage8145en_HK
dc.identifier.eissn1538-7445-
dc.identifier.isiWOS:000260029900053-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung Cheung, AK=25522361600en_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridHung, SC=36798994000en_HK
dc.identifier.scopusauthoridLaw, EWL=36742183700en_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridYau, WL=36914040600en_HK
dc.identifier.scopusauthoridBangarusamy, DK=8948733500en_HK
dc.identifier.scopusauthoridMiller, LD=55728695600en_HK
dc.identifier.scopusauthoridLiu, ETB=7202240109en_HK
dc.identifier.scopusauthoridShao, JY=7201362166en_HK
dc.identifier.scopusauthoridKou, CW=25521877300en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_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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