Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11095
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dc.contributor.authorLouis, Simon N Sen
dc.contributor.authorChow, Laurie T Cen
dc.contributor.authorRezmann, Linda Adrianaen
dc.contributor.authorKrezel, Michael Aen
dc.contributor.authorCatt, Kevin Jen
dc.contributor.authorTikellis, Christosen
dc.contributor.authorFrauman, Albert Gen
dc.contributor.authorLouis, William Jen
dc.date.accessioned2015-05-16T00:40:58Z
dc.date.available2015-05-16T00:40:58Z
dc.date.issued2010-10-01en
dc.identifier.citationThe Prostate; 70(14): 1563-74en
dc.identifier.govdoc20687230en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11095en
dc.description.abstractWe have previously demonstrated Ang II type 2 (AT(2)-) receptor-mediated inhibition of EGF-induced prostate cancer cell growth in androgen-dependent (LNCaP) and independent (PC3) prostate cancer cell lines.To explore the signaling pathways involved in this inhibitory effect, we examined the interaction of the AT(2)-receptor with its novel regulatory partner ATIP using real time PCR, over-expression, siRNA and [(3)H]thymidine incorporation assays.The results in human prostate cancer cell lines demonstrate the presence of ATIP in both cell lines examined, and suggest that (i) the AT(2)-receptor through an interaction with ATIP mediates an anti-growth factor effect in both androgen-dependent and androgen-independent cell lines; (ii) ATIP expression decreases as the rate of cell growth and androgen-independence increase; and (iii) EGF may act on cell growth in part by reducing the content of ATIP present in the cells.The results support our earlier proposal in normal cell lines that ATIP is an important component of the cellular response to AT(2)-receptor activation. The results further suggest that a critical level of ATIP is required to mediate the effect of AT(2)-receptor activation to inhibit EGF mediated increases in cell growth. They also suggest that EGF may in part induce cell growth by suppressing the level of ATIP expression.en
dc.language.isoenen
dc.subject.otherCell Line, Tumoren
dc.subject.otherDNA Primersen
dc.subject.otherEpidermal Growth Factor.pharmacologyen
dc.subject.otherGene Expression Regulation, Neoplasticen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherPolymerase Chain Reactionen
dc.subject.otherProstatic Neoplasms.chemically induced.genetics.metabolismen
dc.subject.otherRNA, Messenger.geneticsen
dc.subject.otherRNA, Small Interfering.geneticsen
dc.subject.otherThymidine.metabolismen
dc.subject.otherTumor Suppressor Proteins.genetics.metabolismen
dc.titleExpression and function of ATIP/MTUS1 in human prostate cancer cell lines.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Prostateen
dc.identifier.affiliationClinical Pharmacology and Therapeutics Unit, University of Melbourne, Department of Medicine, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1002/pros.21192en
dc.description.pages1563-74en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/20687230en
dc.type.austinJournal Articleen
local.name.researcherFrauman, Albert G
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptClinical Pharmacology and Therapeutics-
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