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Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11372
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dc.contributor.authorHe, Hongen
dc.contributor.authorHuynh, Nhien
dc.contributor.authorLiu, Kevin Hen
dc.contributor.authorMalcontenti-Wilson, Caterinaen
dc.contributor.authorZhu, Jinen
dc.contributor.authorChristophi, Christopheren
dc.contributor.authorShulkes, Arthuren
dc.contributor.authorBaldwin, Graham Sen
dc.date.accessioned2015-05-16T00:57:44Z
dc.date.available2015-05-16T00:57:44Z
dc.date.issued2011-11-15en
dc.identifier.citationCancer Letters 2011; 317(1): 65-71en
dc.identifier.govdoc22100495en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11372en
dc.description.abstractThe p21-activated kinase 1 (PAK1) plays important roles in cell growth, motility, and transformation. The aims of this study were to delineate the signalling mechanisms downstream of PAK1, and to investigate the importance of PAK1 for colorectal cancer (CRC) growth and metastasis in vivo. PAK1 knockdown in human CRC cell lines inhibited β-catenin expression, β-catenin/TCF4 transcriptional activity, and the expression of c-Myc. In mouse models PAK1 knockdown suppressed the growth and metastasis of human CRC cells by decreasing proliferation and increasing apoptosis. Our findings demonstrate for the first time the crucial role of PAK1 in CRC progression in vivo.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherApoptosisen
dc.subject.otherBasic Helix-Loop-Helix Leucine Zipper Transcription Factors.metabolismen
dc.subject.otherCell Proliferationen
dc.subject.otherColorectal Neoplasms.enzymology.genetics.pathologyen
dc.subject.otherGene Knockdown Techniquesen
dc.subject.otherHCT116 Cellsen
dc.subject.otherHT29 Cellsen
dc.subject.otherHumansen
dc.subject.otherLiver Neoplasms.enzymology.genetics.secondaryen
dc.subject.otherMiceen
dc.subject.otherMice, SCIDen
dc.subject.otherNeoplasm Invasivenessen
dc.subject.otherProto-Oncogene Proteins c-myc.metabolismen
dc.subject.otherRNA Interferenceen
dc.subject.otherSignal Transductionen
dc.subject.otherTime Factorsen
dc.subject.otherTranscription Factors.metabolismen
dc.subject.otherTransfectionen
dc.subject.otherTumor Burdenen
dc.subject.otherXenograft Model Antitumor Assaysen
dc.subject.otherbeta Catenin.genetics.metabolismen
dc.subject.otherp21-Activated Kinases.deficiency.geneticsen
dc.titleP-21 activated kinase 1 knockdown inhibits β-catenin signalling and blocks colorectal cancer growth.en
dc.typeJournal Articleen
dc.identifier.journaltitleCancer lettersen
dc.identifier.affiliationDepartment of Surgery, University of Melbourne, Austin Health, Heidelberg, Victoria, Australia 3084, Australiaen
dc.identifier.doi10.1016/j.canlet.2011.11.014en
dc.description.pages65-71en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/22100495en
dc.type.austinJournal Articleen
local.name.researcherChristophi, Christopher
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptSurgery (University of Melbourne)-
crisitem.author.deptSurgery-
crisitem.author.deptHepatopancreatobiliary Surgery-
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