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Article: miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion

TitlemiR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion
Authors
Keywordsβ-catenin
Invasion
microRNA
Migration
Nasopharyngeal carcinoma
Issue Date2010
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541 How to Cite?
AbstractNasopharyngeal carcinoma (NPC), a highly metastatic and invasive malignant tumor originating from the nasopharynx, is widely prevalent in Southeast Asia, the Middle East and North Africa. Although viral, dietary and genetic factors have been implicated in NPC, the molecular basis of its pathogenesis is not well defined. Based on a recent microRNA (miRNA) microarray study showing miR-200 downregulation in NPC, we further investigated the role of miR-200a in NPC carcinogenesis. We found that the endogenous miR-200a expression level increases with the degree of differentiation in a panel of NPC cell lines, namely undifferentiated C666-1, high-differentiated CNE-1, and low-differentiated CNE-2 and HNE1 cells. By a series of gain-of-function and loss-of-function studies, we showed that over-expression of miR-200a inhibits C666-1 cell growth, migration and invasion, whereas its knock-down stimulates these processes in CNE-1 cells. In addition, we further identified ZEB2 and CTNNB1 as the functional downstream targets of miR-200a. Interestingly, knock-down of ZEB2 solely impeded NPC cell migration and invasion, whereas CTNNB1 suppression only inhibited NPC cell growth, suggesting that the inhibitory effects of miR-200a on NPC cell growth, migration and invasion are mediated by distinct targets and pathways. Our results reveal the important role of miR-200a as a regulatory factor of NPC carcinogenesis and a potential candidate for miRNA-based therapy against NPC. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/69496
ISSN
2014 Impact Factor: 2.297
2014 SCImago Journal Rankings: 1.006
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Special Administrative Region, China467109
National Basic Research Program of China2010CB529400
2010CB912800
Funding Information:

We thank Mr. Wesley Tucker for critical reading of the paper. This work was Supported by the Research Grants Council of the Hong Kong Special Administrative Region, China (No. 467109). National Basic Research Program of China (973 Program) (Nos. 2010CB529400; 2010CB912800).

References

 

DC FieldValueLanguage
dc.contributor.authorXia, Hen_HK
dc.contributor.authorNg, SSen_HK
dc.contributor.authorJiang, Sen_HK
dc.contributor.authorCheung, WKCen_HK
dc.contributor.authorSze, Jen_HK
dc.contributor.authorBian, XWen_HK
dc.contributor.authorKung, Hfen_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2010-09-06T06:14:12Z-
dc.date.available2010-09-06T06:14:12Z-
dc.date.issued2010en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/69496-
dc.description.abstractNasopharyngeal carcinoma (NPC), a highly metastatic and invasive malignant tumor originating from the nasopharynx, is widely prevalent in Southeast Asia, the Middle East and North Africa. Although viral, dietary and genetic factors have been implicated in NPC, the molecular basis of its pathogenesis is not well defined. Based on a recent microRNA (miRNA) microarray study showing miR-200 downregulation in NPC, we further investigated the role of miR-200a in NPC carcinogenesis. We found that the endogenous miR-200a expression level increases with the degree of differentiation in a panel of NPC cell lines, namely undifferentiated C666-1, high-differentiated CNE-1, and low-differentiated CNE-2 and HNE1 cells. By a series of gain-of-function and loss-of-function studies, we showed that over-expression of miR-200a inhibits C666-1 cell growth, migration and invasion, whereas its knock-down stimulates these processes in CNE-1 cells. In addition, we further identified ZEB2 and CTNNB1 as the functional downstream targets of miR-200a. Interestingly, knock-down of ZEB2 solely impeded NPC cell migration and invasion, whereas CTNNB1 suppression only inhibited NPC cell growth, suggesting that the inhibitory effects of miR-200a on NPC cell growth, migration and invasion are mediated by distinct targets and pathways. Our results reveal the important role of miR-200a as a regulatory factor of NPC carcinogenesis and a potential candidate for miRNA-based therapy against NPC. © 2009 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.subjectβ-cateninen_HK
dc.subjectInvasionen_HK
dc.subjectmicroRNAen_HK
dc.subjectMigrationen_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.titlemiR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=391&issue=1&spage=535&epage=541&date=2009&atitle=miR-200a-mediated+Downregulation+of+ZEB2+and+CTNNB1+Differentially+Inhibits+Nasopharyngeal+Carcinoma+Cell+Growth,+Migration+and+Invasionen_HK
dc.identifier.emailNg, SS: ssmng@hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SS=rp00767en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbrc.2009.11.093en_HK
dc.identifier.pmid19931509en_HK
dc.identifier.scopuseid_2-s2.0-72949119530en_HK
dc.identifier.hkuros168153en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-72949119530&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume391en_HK
dc.identifier.issue1en_HK
dc.identifier.spage535en_HK
dc.identifier.epage541en_HK
dc.identifier.isiWOS:000273624500094-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, H=12545165300en_HK
dc.identifier.scopusauthoridNg, SS=7403358718en_HK
dc.identifier.scopusauthoridJiang, S=36523046900en_HK
dc.identifier.scopusauthoridCheung, WKC=35080070600en_HK
dc.identifier.scopusauthoridSze, J=7003867625en_HK
dc.identifier.scopusauthoridBian, XW=7103023096en_HK
dc.identifier.scopusauthoridKung, Hf=7402514190en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK
dc.identifier.citeulike6197962-

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