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Article: Knockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cells

TitleKnockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cells
Authors
Yu, FNg, SSMChow, BKCSze, JLu, GPoon, WSKung, HFLin, MCM
KeywordsAnti-invasion
Antiproliferation
Cell cycle
Glioma
IFITM1
Issue Date2011
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0167-594X
Citation
Journal Of Neuro-Oncology, 2011, v. 103 n. 2, p. 187-195 How to Cite?
DOI: http://dx.doi.org/10.1007/s11060-010-0377-4
AbstractInterferon-induced transmembrane protein 1 (IFITM1) has recently been identified as a new molecular marker in human colorectal cancer. However, its role in glioma carcinogenesis is not known. In this study, we demonstrated that suppression of IFITM1 expression significantly inhibited proliferation of glioma cells in a time-dependent manner. The growth inhibitory effect was mediated by cell cycle arrest. Furthermore, IFITM1 knockdown significantly inhibited migration and invasion of glioma cells, which could be attributed to decreased expression and enzymatic activity of matrix metalloproteinase 9. Taken together, these results suggest that IFITM1 is a potential therapeutic target for gliomas. © 2010 The Author(s).
Persistent Identifierhttp://hdl.handle.net/10722/145062
ISSN
0167-594X
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.131
PubMed Central ID
PMC3097340
ISI Accession Number ID
WOS:000290773100002
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorYu, Fen_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorChow, BKCen_HK
dc.contributor.authorSze, Jen_HK
dc.contributor.authorLu, Gen_HK
dc.contributor.authorPoon, WSen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCMen_HK
dc.date.accessioned2012-02-21T05:44:17Z-
dc.date.available2012-02-21T05:44:17Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Neuro-Oncology, 2011, v. 103 n. 2, p. 187-195en_HK
dc.identifier.issn0167-594Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/145062-
dc.description.abstractInterferon-induced transmembrane protein 1 (IFITM1) has recently been identified as a new molecular marker in human colorectal cancer. However, its role in glioma carcinogenesis is not known. In this study, we demonstrated that suppression of IFITM1 expression significantly inhibited proliferation of glioma cells in a time-dependent manner. The growth inhibitory effect was mediated by cell cycle arrest. Furthermore, IFITM1 knockdown significantly inhibited migration and invasion of glioma cells, which could be attributed to decreased expression and enzymatic activity of matrix metalloproteinase 9. Taken together, these results suggest that IFITM1 is a potential therapeutic target for gliomas. © 2010 The Author(s).en_HK
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0167-594Xen_HK
dc.relation.ispartofJournal of Neuro-Oncologyen_HK
dc.rightsThe Author(s)en_US
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.en_US
dc.subjectAnti-invasionen_HK
dc.subjectAntiproliferationen_HK
dc.subjectCell cycleen_HK
dc.subjectGliomaen_HK
dc.subjectIFITM1en_HK
dc.titleKnockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4551/resserv?sid=springerlink&genre=article&atitle=Knockdown of interferon-induced transmembrane protein 1 (IFITM1) inhibits proliferation, migration, and invasion of glioma cells&title=Journal of Neuro-Oncology&issn=0167594X&date=2011-06-01&volume=103&issue=2& spage=187&authors=Fang Yu, Samuel S. M. Ng, Billy K. C. Chow, <i>et al.</i>en_US
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailChow, BKC: bkcc@hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s11060-010-0377-4en_HK
dc.identifier.pmid20838853-
dc.identifier.pmcidPMC3097340-
dc.identifier.scopuseid_2-s2.0-79959840536en_HK
dc.identifier.hkuros181308-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959840536&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume103en_HK
dc.identifier.issue2en_HK
dc.identifier.spage187en_HK
dc.identifier.epage195en_HK
dc.identifier.eissn1573-7373en_US
dc.identifier.isiWOS:000290773100002-
dc.publisher.placeUnited Statesen_HK
dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
dc.identifier.scopusauthoridYu, F=36986533000en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK
dc.identifier.scopusauthoridSze, J=7003867625en_HK
dc.identifier.scopusauthoridLu, G=36619108300en_HK
dc.identifier.scopusauthoridPoon, WS=7103025507en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.citeulike7885118-
dc.identifier.issnl0167-594X-

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