Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11133
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dc.contributor.authorKovac, Suzanaen
dc.contributor.authorXiao, Linen
dc.contributor.authorShulkes, Arthuren
dc.contributor.authorPatel, Oneelen
dc.contributor.authorBaldwin, Graham Sen
dc.date.accessioned2015-05-16T00:43:14Z
dc.date.available2015-05-16T00:43:14Z
dc.date.issued2010-10-08en
dc.identifier.citationFebs Letters 2010; 584(21): 4413-8en
dc.identifier.govdoc20932834en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11133en
dc.description.abstractThe involvement of the gastrointestinal hormone gastrin in the development of gastrointestinal cancer is highly controversial. Here we demonstrate a positive-feedback loop whereby gastrin, acting via the CCK2 receptor, increases its own expression. Such an autocrine loop has not previously been reported for any other gastrointestinal hormone. Gastrin promoter activation was dependent on the MAP kinase pathway and did not involve Sp1 binding sites or epidermal growth factor receptor transactivation. As the treatment of gastrointestinal cancer cells with amidated gastrin led to increased expression of non-amidated gastrins, the positive-feedback loop may contribute to the sustained increase in circulating gastrins observed in colorectal cancer patients.en
dc.language.isoenen
dc.subject.otherBase Sequenceen
dc.subject.otherCell Line, Tumoren
dc.subject.otherColorectal Neoplasms.blood.genetics.metabolismen
dc.subject.otherFeedback, Physiologicalen
dc.subject.otherGastrins.biosynthesis.blood.genetics.metabolismen
dc.subject.otherGastrointestinal Neoplasms.genetics.metabolism.pathologyen
dc.subject.otherGene Expression Regulation, Neoplasticen
dc.subject.otherGenes, Reporter.geneticsen
dc.subject.otherHumansen
dc.subject.otherLuciferases.geneticsen
dc.subject.otherMAP Kinase Signaling Systemen
dc.subject.otherMolecular Sequence Dataen
dc.subject.otherPolymerase Chain Reactionen
dc.subject.otherPromoter Regions, Genetic.geneticsen
dc.subject.otherReceptor, Cholecystokinin B.metabolismen
dc.subject.otherTime Factorsen
dc.subject.otherTranscription, Geneticen
dc.subject.otherTranscriptional Activationen
dc.titleGastrin increases its own synthesis in gastrointestinal cancer cells via the CCK2 receptor.en
dc.typeJournal Articleen
dc.identifier.journaltitleFEBS lettersen
dc.identifier.affiliationThe University of Melbourne, Department of Surgery, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1016/j.febslet.2010.09.046en
dc.description.pages4413-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/20932834en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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