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Article: LTBP-2 confers pleiotropic suppression and promotes dormancy in a growth factor permissive microenvironment in nasopharyngeal carcinoma

TitleLTBP-2 confers pleiotropic suppression and promotes dormancy in a growth factor permissive microenvironment in nasopharyngeal carcinoma
Authors
KeywordsAnti-angiogenesis
Latent transforming growth factor β binding protein 2 (LTBP-2)
Metastatic growth
Nasopharyngeal carcinoma (NPC)
Tumor cell dormancy
Tumor suppression
Issue Date2012
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2012, v. 325 n. 1, p. 89-98 How to Cite?
Abstract
This study identified LTBP-2 as a pleiotropic tumor suppressor in nasopharyngeal carcinoma, which safeguards against critical malignant behaviors of tumor cells. LTBP-2 expression was significantly decreased or lost in up to 100% of NPC cell lines (7/7) and 80% of biopsies (24/30). Promoter hypermethylation was found to be involved in LTBP-2 silencing. Using a tetracycline-regulated inducible expression system, we unveiled functional roles of LTBP-2 in suppressing colony formation, anchorage-independent growth, cell migration, angiogenesis, VEGF secretion, and tumorigenicity. Three-dimensional culture studies suggested the involvement of LTBP-2 in maintenance of tumor cell dormancy in a growth factor favorable microenvironment. © 2012 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/159266
ISSN
2013 Impact Factor: 5.016
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Hen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorWong, VCLen_HK
dc.contributor.authorHyytiainen, Men_HK
dc.contributor.authorKeskiOja, Jen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorCheung, FMFen_HK
dc.contributor.authorLee, AWMen_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorZabarovsky, ERen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorTao, Qen_HK
dc.contributor.authorKan, Ren_HK
dc.contributor.authorChan, SHKen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2012-08-16T05:47:33Z-
dc.date.available2012-08-16T05:47:33Z-
dc.date.issued2012en_HK
dc.identifier.citationCancer Letters, 2012, v. 325 n. 1, p. 89-98en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/159266-
dc.description.abstractThis study identified LTBP-2 as a pleiotropic tumor suppressor in nasopharyngeal carcinoma, which safeguards against critical malignant behaviors of tumor cells. LTBP-2 expression was significantly decreased or lost in up to 100% of NPC cell lines (7/7) and 80% of biopsies (24/30). Promoter hypermethylation was found to be involved in LTBP-2 silencing. Using a tetracycline-regulated inducible expression system, we unveiled functional roles of LTBP-2 in suppressing colony formation, anchorage-independent growth, cell migration, angiogenesis, VEGF secretion, and tumorigenicity. Three-dimensional culture studies suggested the involvement of LTBP-2 in maintenance of tumor cell dormancy in a growth factor favorable microenvironment. © 2012 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.subjectAnti-angiogenesisen_HK
dc.subjectLatent transforming growth factor β binding protein 2 (LTBP-2)en_HK
dc.subjectMetastatic growthen_HK
dc.subjectNasopharyngeal carcinoma (NPC)en_HK
dc.subjectTumor cell dormancyen_HK
dc.subjectTumor suppressionen_HK
dc.titleLTBP-2 confers pleiotropic suppression and promotes dormancy in a growth factor permissive microenvironment in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailChua, D: dttchua@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2012.06.005en_HK
dc.identifier.pmid22743615-
dc.identifier.scopuseid_2-s2.0-84865283257en_HK
dc.identifier.hkuros202596en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84865283257&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume325en_HK
dc.identifier.issue1en_HK
dc.identifier.spage89en_HK
dc.identifier.epage98en_HK
dc.identifier.isiWOS:000308781600011-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridChen, H=37090169400en_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridWong, VCL=23096631300en_HK
dc.identifier.scopusauthoridHyytiainen, M=6507430668en_HK
dc.identifier.scopusauthoridKeskiOja, J=7005572715en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridCheung, FMF=55311344600en_HK
dc.identifier.scopusauthoridLee, AWM=17035384900en_HK
dc.identifier.scopusauthoridKwong, DLW=54890371000en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridZabarovsky, ER=7007009108en_HK
dc.identifier.scopusauthoridTsao, SW=55311525100en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.scopusauthoridKan, R=55311455200en_HK
dc.identifier.scopusauthoridChan, SHK=55244046300en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.citeulike11279395-

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