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Article: Tumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype
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TitleTumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype
 
AuthorsWong, VCL2
Chen, H4
Ko, JMY2
Chan, KW2
Chan, YP2
Law, S2
Chua, D2
Kwong, DLW2
Lung, HL2
Srivastava, G2
Tang, JCO3
Tsao, SW2
Zabarovsky, ER1 6
Stanbridge, EJ5
Lung, ML2
 
Keywordsdual-specificity phosphatase 6 (DUSP6)
tumor suppression
 
Issue Date2012
 
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
CitationInternational Journal Of Cancer, 2012, v. 130 n. 1, p. 83-95 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.25970
 
AbstractSuppressive effects of DUSP6 in tumorigenesis and EMT-associated properties were observed. Dual-specificity phosphatase (DUSP6) is a MAP kinase phosphatase (MKP) negatively regulating the activity of ERK, one of the major molecular switches in the MAPK signaling cascade propagating the signaling responses during malignancies. The impact of DUSP6 in EMT and its contribution to tumor dissemination has not yet been characterized. Due to differences in tumor microenvironments affecting cell signaling during cancer progression, DUSP6 may play varying roles in tumor development. We sought to examine the potential role of DUSP6-mediated tumorigenesis and EMT-associated properties in two aerodigestive tract cancers, namely, esophageal squamous cell carcinoma (ESCC) and nasopharyngeal carcinoma (NPC). Significant loss of DUSP6 was observed in 100% of 11 ESCC cell lines and 71% of seven NPC cell lines. DUSP6 expression was down-regulated in 40% of 30 ESCC tumor tissues and 75% of 20 NPC tumor tissues compared to their respective normal counterparts. Suppressive effects of DUSP6 in tumor formation and cancer cell mobility are seen in in vivo tumorigenicity assay and in vitro colony formation, three-dimensional Matrigel culture, cell migration and invasion chamber tests. Notably, overexpression of DUSP6 impairs EMT-associated properties. Furthermore, tissue microarray analysis reveals a clinical association of DUSP6 expression with better patient survival. Taken together, our study provides a novel insight into understanding the functional impact of DUSP6 in tumorigenesis and metastasis of ESCC and NPC. Copyright © 2011 UICC.
 
ISSN0020-7136
2013 Impact Factor: 5.007
 
DOIhttp://dx.doi.org/10.1002/ijc.25970
 
ISI Accession Number IDWOS:000297851300009
Funding AgencyGrant Number
University Grants Council
University of Hong Kong
Swedish Cancer Society
Swedish Research Council
Swedish Institute, Karolinska Institute
Funding Information:

Grant sponsors: The University Grants Council Area of Excellence grant and the University of Hong Kong Seed Funding (MLL) Programme for Basic Research, the Swedish Cancer Society, the Swedish Research Council, the Swedish Institute, Karolinska Institute (ERZ)

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWong, VCL
 
dc.contributor.authorChen, H
 
dc.contributor.authorKo, JMY
 
dc.contributor.authorChan, KW
 
dc.contributor.authorChan, YP
 
dc.contributor.authorLaw, S
 
dc.contributor.authorChua, D
 
dc.contributor.authorKwong, DLW
 
dc.contributor.authorLung, HL
 
dc.contributor.authorSrivastava, G
 
dc.contributor.authorTang, JCO
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorZabarovsky, ER
 
dc.contributor.authorStanbridge, EJ
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2012-02-03T06:11:43Z
 
dc.date.available2012-02-03T06:11:43Z
 
dc.date.issued2012
 
dc.description.abstractSuppressive effects of DUSP6 in tumorigenesis and EMT-associated properties were observed. Dual-specificity phosphatase (DUSP6) is a MAP kinase phosphatase (MKP) negatively regulating the activity of ERK, one of the major molecular switches in the MAPK signaling cascade propagating the signaling responses during malignancies. The impact of DUSP6 in EMT and its contribution to tumor dissemination has not yet been characterized. Due to differences in tumor microenvironments affecting cell signaling during cancer progression, DUSP6 may play varying roles in tumor development. We sought to examine the potential role of DUSP6-mediated tumorigenesis and EMT-associated properties in two aerodigestive tract cancers, namely, esophageal squamous cell carcinoma (ESCC) and nasopharyngeal carcinoma (NPC). Significant loss of DUSP6 was observed in 100% of 11 ESCC cell lines and 71% of seven NPC cell lines. DUSP6 expression was down-regulated in 40% of 30 ESCC tumor tissues and 75% of 20 NPC tumor tissues compared to their respective normal counterparts. Suppressive effects of DUSP6 in tumor formation and cancer cell mobility are seen in in vivo tumorigenicity assay and in vitro colony formation, three-dimensional Matrigel culture, cell migration and invasion chamber tests. Notably, overexpression of DUSP6 impairs EMT-associated properties. Furthermore, tissue microarray analysis reveals a clinical association of DUSP6 expression with better patient survival. Taken together, our study provides a novel insight into understanding the functional impact of DUSP6 in tumorigenesis and metastasis of ESCC and NPC. Copyright © 2011 UICC.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationInternational Journal Of Cancer, 2012, v. 130 n. 1, p. 83-95 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.25970
 
dc.identifier.doihttp://dx.doi.org/10.1002/ijc.25970
 
dc.identifier.epage95
 
dc.identifier.hkuros198360
 
dc.identifier.isiWOS:000297851300009
Funding AgencyGrant Number
University Grants Council
University of Hong Kong
Swedish Cancer Society
Swedish Research Council
Swedish Institute, Karolinska Institute
Funding Information:

Grant sponsors: The University Grants Council Area of Excellence grant and the University of Hong Kong Seed Funding (MLL) Programme for Basic Research, the Swedish Cancer Society, the Swedish Research Council, the Swedish Institute, Karolinska Institute (ERZ)

 
dc.identifier.issn0020-7136
2013 Impact Factor: 5.007
 
dc.identifier.issue1
 
dc.identifier.pmid21387288
 
dc.identifier.scopuseid_2-s2.0-79952279912
 
dc.identifier.spage83
 
dc.identifier.urihttp://hdl.handle.net/10722/144512
 
dc.identifier.volume130
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
dc.publisher.placeUnited States
 
dc.relation.ispartofInternational Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc..
 
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - pathology
 
dc.subject.meshDual Specificity Phosphatase 6 - genetics - metabolism
 
dc.subject.meshEpithelial-Mesenchymal Transition
 
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathology
 
dc.subject.meshNasopharyngeal Neoplasms - genetics - metabolism - pathology
 
dc.subjectdual-specificity phosphatase 6 (DUSP6)
 
dc.subjecttumor suppression
 
dc.titleTumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype
 
dc.typeArticle
 
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Author Affiliations
  1. Karolinska University Hospital
  2. The University of Hong Kong
  3. Hong Kong Polytechnic University
  4. Hong Kong University of Science and Technology
  5. UC Irvine
  6. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences