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Article: The ECM protein LTBP-2 is a suppressor of esophageal squamous cell carcinoma tumor formation but higher tumor expression associates with poor patient outcome

TitleThe ECM protein LTBP-2 is a suppressor of esophageal squamous cell carcinoma tumor formation but higher tumor expression associates with poor patient outcome
Authors
Keywordsantiangiogenesis
ESCC
extracellular matrix protein
hypermethylation
invasion
LOH
LTBP-2
microcell-mediated chromosome transfer
migration
tumor suppressor gene
Issue Date2011
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2011, v. 129 n. 3, p. 565-573 How to Cite?
AbstractOur previous studies of chromosome 14 transfer into tumorigenic esophageal squamous cell carcinoma (ESCC) cell line, SLMT, suggested the existence of tumor suppressor genes on chromosome 14. Gene expression profiling of microcell hybrids and the tumor segregants identified an interesting gene, LTBP-2 (latent transforming growth factor β binding protein 2), which has been analyzed here for its role in ESCC. LTBP-2 maps to 14q24 and encodes a secreted protein, which is a component of the extracellular matrix microfibrils. LTBP-2 expression was downregulated in ESCC cell lines and tumor tissues. Promoter hypermethylation was found to be involved in LTBP-2 inactivation. Functional studies indicated its tumor-suppressive roles in ESCC. In the in vitro colony formation and Matrigel three-dimensional culture assays, LTBP-2 decreased the colony-forming abilities of ESCC cell lines. LTBP-2 expression was associated with reduction of cell migrating and invasive abilities. LTBP-2 could also reduce the tube-forming ability of endothelial cells. Moreover, LTBP-2 induced tumor suppression in in vivo nude mouse assays. Tissue microarray immunohistochemical staining analysis indicated that LTBP-2 expression is reduced in tumor tissues when compared to normal tissues, and LTBP-2 expression correlated significantly with the survival of ESCC patients. Thus, LTBP-2 appears to play an important role in ESCC. Copyright © 2010 UICC.
Persistent Identifierhttp://hdl.handle.net/10722/137199
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of ChinaHKU 3/06C
Funding Information:

Grant sponsor: Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of China; Grant number: HKU 3/06C (Collaborative Research Fund on "Esophageal Carcinoma Research Center'')

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorChan, SHKen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorTao, Qen_HK
dc.contributor.authorHyytiainen, Men_HK
dc.contributor.authorKeskiOja, Jen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorTang, Jen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorChen, Hen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2011-08-26T14:18:43Z-
dc.date.available2011-08-26T14:18:43Z-
dc.date.issued2011en_HK
dc.identifier.citationInternational Journal Of Cancer, 2011, v. 129 n. 3, p. 565-573en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137199-
dc.description.abstractOur previous studies of chromosome 14 transfer into tumorigenic esophageal squamous cell carcinoma (ESCC) cell line, SLMT, suggested the existence of tumor suppressor genes on chromosome 14. Gene expression profiling of microcell hybrids and the tumor segregants identified an interesting gene, LTBP-2 (latent transforming growth factor β binding protein 2), which has been analyzed here for its role in ESCC. LTBP-2 maps to 14q24 and encodes a secreted protein, which is a component of the extracellular matrix microfibrils. LTBP-2 expression was downregulated in ESCC cell lines and tumor tissues. Promoter hypermethylation was found to be involved in LTBP-2 inactivation. Functional studies indicated its tumor-suppressive roles in ESCC. In the in vitro colony formation and Matrigel three-dimensional culture assays, LTBP-2 decreased the colony-forming abilities of ESCC cell lines. LTBP-2 expression was associated with reduction of cell migrating and invasive abilities. LTBP-2 could also reduce the tube-forming ability of endothelial cells. Moreover, LTBP-2 induced tumor suppression in in vivo nude mouse assays. Tissue microarray immunohistochemical staining analysis indicated that LTBP-2 expression is reduced in tumor tissues when compared to normal tissues, and LTBP-2 expression correlated significantly with the survival of ESCC patients. Thus, LTBP-2 appears to play an important role in ESCC. Copyright © 2010 UICC.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc..-
dc.subjectantiangiogenesisen_HK
dc.subjectESCCen_HK
dc.subjectextracellular matrix proteinen_HK
dc.subjecthypermethylationen_HK
dc.subjectinvasionen_HK
dc.subjectLOHen_HK
dc.subjectLTBP-2en_HK
dc.subjectmicrocell-mediated chromosome transferen_HK
dc.subjectmigrationen_HK
dc.subjecttumor suppressor geneen_HK
dc.subject.meshCarcinoma, Squamous Cell - metabolism - mortality-
dc.subject.meshEsophageal Neoplasms - metabolism - mortality-
dc.subject.meshGenes, Tumor Suppressor-
dc.subject.meshLatent TGF-beta Binding Proteins - genetics - metabolism-
dc.subject.meshNeoplasm Transplantation-
dc.titleThe ECM protein LTBP-2 is a suppressor of esophageal squamous cell carcinoma tumor formation but higher tumor expression associates with poor patient outcomeen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.25698en_HK
dc.identifier.pmid20878956-
dc.identifier.scopuseid_2-s2.0-79958026767en_HK
dc.identifier.hkuros191277en_US
dc.identifier.hkuros196090en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958026767&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume129en_HK
dc.identifier.issue3en_HK
dc.identifier.spage565en_HK
dc.identifier.epage573en_HK
dc.identifier.isiWOS:000291606000006-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridChan, SHK=55244046300en_HK
dc.identifier.scopusauthoridYee Ko, JM=39262799100en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.scopusauthoridHyytiainen, M=6507430668en_HK
dc.identifier.scopusauthoridKeskiOja, J=7005572715en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridTang, J=14056850300en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridChen, H=37090169400en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.citeulike7948528-

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