Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9342
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dc.contributor.authorLeng, S Len
dc.contributor.authorLeeding, K Sen
dc.contributor.authorGibson, P Ren
dc.contributor.authorBach, Leon Aen
dc.date.accessioned2015-05-15T22:24:15Z
dc.date.available2015-05-15T22:24:15Z
dc.date.issued2001-10-01en
dc.identifier.citationCarcinogenesis; 22(10): 1625-31en
dc.identifier.govdoc11577001en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9342en
dc.description.abstractButyrate has potent anti-tumorigenic effects on many colon cancer cell lines, including inhibition of growth and promotion of apoptosis in vitro. Nevertheless, despite the butyrate concentration in the colonic lumen being sufficient to result in the death of almost all cells in vitro, colon cancers still develop and grow in vivo, suggesting that cancer cells must develop mechanisms by which they escape the effects of butyrate observed in vitro. Insulin-like growth factor-II (IGF-II) is an autocrine growth factor in many colon cancer cells. The aim of this study was to determine whether IGF-II influences butyrate-mediated apoptosis in LIM 2405 human colon cancer cells. Butyrate and trichostatin A, both of which are histone deacetylase inhibitors although the latter is more specific, induced apoptosis as determined by floating cell counting, Hoechst 33258 staining, DNA laddering and a cell death detection ELISA. IGF-II inhibited the effects of both agents. Butyrate but not trichostatin A also induced LIM 2405 cell migration. In contrast to the above results, IGF-II enhanced butyrate-induced cell migration. Levels of IGF binding protein-3 (IGFBP-3), which may induce apoptosis by IGF-dependent or -independent mechanisms, were increased by butyrate and trichostatin A; IGF-II augmented this effect. It is therefore unlikely that IGFBP-3 mediates butyrate-induced apoptosis. We suggest that IGF-II inhibits the pro-apoptotic effect of butyrate downstream of histone deacetylase inhibition. In contrast, IGF-II promotes histone deacetylase-dependent IGFBP-3 expression and histone deacetylase-independent migration. IGF-II may promote tumour growth by mediating the development of resistance to the pro-apoptotic effects of butyrate.en
dc.language.isoenen
dc.subject.otherApoptosis.drug effectsen
dc.subject.otherBisbenzimidazole.diagnostic useen
dc.subject.otherBlotting, Westernen
dc.subject.otherButyrates.pharmacologyen
dc.subject.otherCell Movement.drug effectsen
dc.subject.otherCell Survival.drug effectsen
dc.subject.otherColonic Neoplasms.pathologyen
dc.subject.otherDrug Resistance, Neoplasmen
dc.subject.otherEnzyme Inhibitors.pharmacologyen
dc.subject.otherEnzyme-Linked Immunosorbent Assayen
dc.subject.otherGene Expression Regulation.drug effectsen
dc.subject.otherHistone Deacetylase Inhibitorsen
dc.subject.otherHumansen
dc.subject.otherHydroxamic Acids.pharmacologyen
dc.subject.otherImmunoblottingen
dc.subject.otherInsulin-Like Growth Factor Binding Protein 3.metabolismen
dc.subject.otherInsulin-Like Growth Factor II.metabolism.pharmacologyen
dc.subject.otherRNA, Messenger.analysisen
dc.subject.otherTumor Cells, Cultured.drug effects.pathologyen
dc.titleInsulin-like growth factor-II renders LIM 2405 human colon cancer cells resistant to butyrate-induced apoptosis: a potential mechanism for colon cancer cell survival in vivo.en
dc.typeJournal Articleen
dc.identifier.journaltitleCarcinogenesisen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin & Repatriation Medical Centre, Studley Road, Heidelberg, Australiaen
dc.description.pages1625-31en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11577001en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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