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Article: miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion
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TitlemiR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion
 
AuthorsXia, H2
Ng, SS2
Jiang, S3
Cheung, WKC2
Sze, J2
Bian, XW4
Kung, Hf1 3
Lin, MC2
 
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
 
CitationBiochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbrc.2009.11.093
 
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.
 
ISSN0006-291X
2013 Impact Factor: 2.281
 
DOIhttp://dx.doi.org/10.1016/j.bbrc.2009.11.093
 
ISI Accession Number IDWOS:000273624500094
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).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, H
 
dc.contributor.authorNg, SS
 
dc.contributor.authorJiang, S
 
dc.contributor.authorCheung, WKC
 
dc.contributor.authorSze, J
 
dc.contributor.authorBian, XW
 
dc.contributor.authorKung, Hf
 
dc.contributor.authorLin, MC
 
dc.date.accessioned2010-09-06T06:14:12Z
 
dc.date.available2010-09-06T06:14:12Z
 
dc.date.issued2010
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationBiochemical And Biophysical Research Communications, 2010, v. 391 n. 1, p. 535-541 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bbrc.2009.11.093
 
dc.identifier.citeulike6197962
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.bbrc.2009.11.093
 
dc.identifier.epage541
 
dc.identifier.hkuros168153
 
dc.identifier.isiWOS:000273624500094
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).

 
dc.identifier.issn0006-291X
2013 Impact Factor: 2.281
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid19931509
 
dc.identifier.scopuseid_2-s2.0-72949119530
 
dc.identifier.spage535
 
dc.identifier.urihttp://hdl.handle.net/10722/69496
 
dc.identifier.volume391
 
dc.languageeng
 
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBiochemical and Biophysical Research Communications
 
dc.relation.referencesReferences in Scopus
 
dc.subjectβ-catenin
 
dc.subjectInvasion
 
dc.subjectmicroRNA
 
dc.subjectMigration
 
dc.subjectNasopharyngeal carcinoma
 
dc.titlemiR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion
 
dc.typeArticle
 
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Author Affiliations
  1. Li Ka Shing Institute of Health Sciences
  2. Institute of Molecular Technology for Drug Discovery and Synthesis, Hong Kong
  3. Sun Yat-Sen University
  4. Southwestern Hospital Chongqing