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Article: Id-1 induces cell invasiveness in immortalized epithelial cells by regulating cadherin switching and rho GTPases

TitleId-1 induces cell invasiveness in immortalized epithelial cells by regulating cadherin switching and rho GTPases
Authors
KeywordsEMT
Esophageal
ID-1
Invasiveness
N-Cadherin
Rho GtPases
Issue Date2011
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
Citation
Journal Of Cellular Biochemistry, 2011, v. 112 n. 1, p. 157-168 How to Cite?
AbstractEpithelial-mesenchymal transition (EMT), characterized by cadherin switching, contributes to cancer metastasis. Our recent study showed that Id-1 (inhibitor of differentiation-1) promotes metastasis in esophageal cancer cells, but whether the invasive and metastatic dynamics can be induced early in the carcinogenesis process is still unclear. Immortalization is regarded as the initial stage in the malignant transformation of normal cells. In this study, we investigated the role and mechanisms of Id-1 in inducing EMT and cell invasiveness in immortalized esophageal epithelial cells. We found that immortalized epithelial cells expressed higher endogenous levels of Id-1 compared with normal cells. Ectopic Id-1 expression inhibited the differentiation of immortalized esophageal epithelial cells and promoted cadherin switching, which was accompanied by increased adhesiveness to extracellular matrix, cell motility, migratory potential and matrix metalloproteinase-dependent invasiveness. GTPase activity assays showed that over-expression or short-hairpin RNA knockdown of Id-1 led to corresponding changes in Rac1 activity, whereas RhoA activity was significantly decreased with Id-1 depletion. Inhibitors targeting Rac1, RhoA, and Rho kinase suppressed the invasiveness of Id-1-expressing NE2-hTERT cells. Knockdown of N-cadherin in Id-1-over-expressing cells inhibited cell invasiveness and down-regulated RhoA activity. These data suggest that the Id-1-induced invasive potential may be regulated through the N-cadherin-RhoA axis and Rac1 activation. © 2010 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/142312
ISSN
2015 Impact Factor: 3.446
2015 SCImago Journal Rankings: 1.520
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong Kong Special Administrative RegionHKU 7556/06M
HKUST 2/06C
Research Grants Council of Hong Kong Special Administrative Region, ChinaHKU 7556/06M
HKUST 2/06C
Funding Information:

Grant sponsor: Research Grants Council of Hong Kong Special Administrative Region HKU 7556/06M, HKUST 2/06C.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorCheung, PYen_HK
dc.contributor.authorYip, YLen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2011-10-28T02:42:42Z-
dc.date.available2011-10-28T02:42:42Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Cellular Biochemistry, 2011, v. 112 n. 1, p. 157-168en_HK
dc.identifier.issn0730-2312en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142312-
dc.description.abstractEpithelial-mesenchymal transition (EMT), characterized by cadherin switching, contributes to cancer metastasis. Our recent study showed that Id-1 (inhibitor of differentiation-1) promotes metastasis in esophageal cancer cells, but whether the invasive and metastatic dynamics can be induced early in the carcinogenesis process is still unclear. Immortalization is regarded as the initial stage in the malignant transformation of normal cells. In this study, we investigated the role and mechanisms of Id-1 in inducing EMT and cell invasiveness in immortalized esophageal epithelial cells. We found that immortalized epithelial cells expressed higher endogenous levels of Id-1 compared with normal cells. Ectopic Id-1 expression inhibited the differentiation of immortalized esophageal epithelial cells and promoted cadherin switching, which was accompanied by increased adhesiveness to extracellular matrix, cell motility, migratory potential and matrix metalloproteinase-dependent invasiveness. GTPase activity assays showed that over-expression or short-hairpin RNA knockdown of Id-1 led to corresponding changes in Rac1 activity, whereas RhoA activity was significantly decreased with Id-1 depletion. Inhibitors targeting Rac1, RhoA, and Rho kinase suppressed the invasiveness of Id-1-expressing NE2-hTERT cells. Knockdown of N-cadherin in Id-1-over-expressing cells inhibited cell invasiveness and down-regulated RhoA activity. These data suggest that the Id-1-induced invasive potential may be regulated through the N-cadherin-RhoA axis and Rac1 activation. © 2010 Wiley-Liss, Inc.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503en_HK
dc.relation.ispartofJournal of Cellular Biochemistryen_HK
dc.rightsJournal of Cellular Biochemistry. Copyright © John Wiley & Sons, Inc.en_US
dc.rightsSpecial Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)en_US
dc.subjectEMTen_HK
dc.subjectEsophagealen_HK
dc.subjectID-1en_HK
dc.subjectInvasivenessen_HK
dc.subjectN-Cadherinen_HK
dc.subjectRho GtPasesen_HK
dc.subject.meshCadherins - metabolism-
dc.subject.meshCell Movement-
dc.subject.meshEpithelial-Mesenchymal Transition-
dc.subject.meshInhibitor of Differentiation Protein 1 - metabolism-
dc.subject.meshrho GTP-Binding Proteins - metabolism-
dc.titleId-1 induces cell invasiveness in immortalized epithelial cells by regulating cadherin switching and rho GTPasesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0730-2312&volume=112&issue=1&spage=157&epage=168&date=2011&atitle=Id-1+induces+cell+invasiveness+in+immortalized+epithelial+cells+by+regulating+cadherin+switching+and+Rho+GTPasesen_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jcb.22911en_HK
dc.identifier.pmid21053361-
dc.identifier.scopuseid_2-s2.0-78651267765en_HK
dc.identifier.hkuros184646en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78651267765&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume112en_HK
dc.identifier.issue1en_HK
dc.identifier.spage157en_HK
dc.identifier.epage168en_HK
dc.identifier.isiWOS:000287216200016-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectCentromeric instability in human cells undergoing immortalization: implication for progression of chromosomal instability in carcinogenesis-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridCheung, PY=46061920500en_HK
dc.identifier.scopusauthoridYip, YL=7005596403en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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