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Article: Tumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype

TitleTumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype
Authors
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
Citation
International Journal Of Cancer, 2012, v. 130 n. 1, p. 83-95 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/144512
ISSN
2014 Impact Factor: 5.085
ISI Accession Number ID
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)

References

 

DC FieldValueLanguage
dc.contributor.authorWong, VCLen_HK
dc.contributor.authorChen, Hen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, YPen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorLung, HLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorTang, JCOen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorZabarovsky, ERen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2012-02-03T06:11:43Z-
dc.date.available2012-02-03T06:11:43Z-
dc.date.issued2012en_HK
dc.identifier.citationInternational Journal Of Cancer, 2012, v. 130 n. 1, p. 83-95en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144512-
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.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc..-
dc.subjectdual-specificity phosphatase 6 (DUSP6)en_HK
dc.subjecttumor suppressionen_HK
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.titleTumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotypeen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailChua, D: dttchua@hkucc.hku.hken_HK
dc.identifier.emailKwong, DLW: dlwkwong@hku.hken_HK
dc.identifier.emailLung, HL: hllung2@hku.hken_HK
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityKwong, DLW=rp00414en_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.25970en_HK
dc.identifier.pmid21387288en_HK
dc.identifier.scopuseid_2-s2.0-79952279912en_HK
dc.identifier.hkuros198360en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952279912&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume130en_HK
dc.identifier.issue1en_HK
dc.identifier.spage83en_HK
dc.identifier.epage95en_HK
dc.identifier.isiWOS:000297851300009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, VCL=23096631300en_HK
dc.identifier.scopusauthoridChen, H=37090169400en_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridChan, YP=14009821700en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_HK
dc.identifier.scopusauthoridKwong, DLW=15744231600en_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridTang, JCO=14056850300en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridZabarovsky, ER=7007009108en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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