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Article: EFA6A enhances glioma cell invasion through ADP ribosylation factor 6/extracellular signal-regulated kinase signaling

TitleEFA6A enhances glioma cell invasion through ADP ribosylation factor 6/extracellular signal-regulated kinase signaling
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2006, v. 66 n. 3, p. 1583-1590 How to Cite?
AbstractEFA6A, or Pleckstrin and Sec7 domain protein, is a member of guanine nucleotide exchange factors for ADP ribosylation factor 6 (ARF6). Whereas EFA6A is specifically expressed in the brain, little is known about its function in glial cells or glioma. Here we show that elevated EFA6A expression is detectable in both low-grade and high-grade human glioma tissues samples. To investigate the role of EFA6A in glioma carcinogenesis, we generated a human glioblastoma cell line which conditionally overexpresses EFA6A (U373-EFA6A). We showed that overexpression of EFA6A had no effect on cell proliferation, apoptosis, or cell cycle control. However, as shown by wound healing and in vitro cell invasion assays, it significantly enhanced the cell motility and invasiveness whereas silencing EFA6A by its dominant negative mutant EFA6A(E242K) produced opposite effects. We further showed that ARF6/extracellular signal-regulated kinase (ERK) signaling is required for the EFA6A-mediated cell invasion because both EFA6A(E242K) and ARF6 dominant negative mutant ARF6(T27N) markedly reduced the phosphorylated ERK level and EFA6A-mediated invasive capacity. Consistently, mitogen-activated protein kinase/ERK kinase inhibitor U0126 could abolish the EFA6A-induced cell invasion. These results suggest for the first time a potential role of EFA6A/ARF6/ERK signal cascade in glioma cell migration and invasion. ©2006 American Association for Cancer Research.
DescriptionLi M. and Ng S.M. are equal first authors
Persistent Identifierhttp://hdl.handle.net/10722/148449
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Men_HK
dc.contributor.authorNg, SSMen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorLai, Len_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorFranco, Men_HK
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCMen_HK
dc.date.accessioned2012-05-29T06:13:03Z-
dc.date.available2012-05-29T06:13:03Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Research, 2006, v. 66 n. 3, p. 1583-1590en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148449-
dc.descriptionLi M. and Ng S.M. are equal first authors-
dc.description.abstractEFA6A, or Pleckstrin and Sec7 domain protein, is a member of guanine nucleotide exchange factors for ADP ribosylation factor 6 (ARF6). Whereas EFA6A is specifically expressed in the brain, little is known about its function in glial cells or glioma. Here we show that elevated EFA6A expression is detectable in both low-grade and high-grade human glioma tissues samples. To investigate the role of EFA6A in glioma carcinogenesis, we generated a human glioblastoma cell line which conditionally overexpresses EFA6A (U373-EFA6A). We showed that overexpression of EFA6A had no effect on cell proliferation, apoptosis, or cell cycle control. However, as shown by wound healing and in vitro cell invasion assays, it significantly enhanced the cell motility and invasiveness whereas silencing EFA6A by its dominant negative mutant EFA6A(E242K) produced opposite effects. We further showed that ARF6/extracellular signal-regulated kinase (ERK) signaling is required for the EFA6A-mediated cell invasion because both EFA6A(E242K) and ARF6 dominant negative mutant ARF6(T27N) markedly reduced the phosphorylated ERK level and EFA6A-mediated invasive capacity. Consistently, mitogen-activated protein kinase/ERK kinase inhibitor U0126 could abolish the EFA6A-induced cell invasion. These results suggest for the first time a potential role of EFA6A/ARF6/ERK signal cascade in glioma cell migration and invasion. ©2006 American Association for Cancer Research.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAdp-Ribosylation Factors - Metabolismen_US
dc.subject.meshCell Cycle - Physiologyen_US
dc.subject.meshCell Growth Processes - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movement - Physiologyen_US
dc.subject.meshDoxycycline - Pharmacologyen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshGlioblastoma - Genetics - Metabolism - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMap Kinase Signaling Systemen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshNerve Tissue Proteins - Biosynthesis - Genetics - Physiologyen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshRna, Messenger - Biosynthesis - Geneticsen_US
dc.subject.meshTransfectionen_US
dc.titleEFA6A enhances glioma cell invasion through ADP ribosylation factor 6/extracellular signal-regulated kinase signalingen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, SSM: ssmng@hku.hken_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailLeung, SY: suetyi@hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SSM=rp00767en_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1158/0008-5472.CAN-05-2424en_HK
dc.identifier.pmid16452216-
dc.identifier.scopuseid_2-s2.0-32944471558en_HK
dc.identifier.hkuros114253-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-32944471558&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1583en_HK
dc.identifier.epage1590en_HK
dc.identifier.isiWOS:000235095900043-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, M=36067425800en_HK
dc.identifier.scopusauthoridNg, SSM=7403358718en_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridLai, L=12445800200en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridFranco, M=7202646998en_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.customcontrol.immutablesml 130621-

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