Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/19599
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dc.contributor.authorLuk, Ian Y-
dc.contributor.authorReehorst, Camilla M-
dc.contributor.authorMariadason, John M-
dc.date2018-08-30-
dc.date.accessioned2018-10-11T02:51:45Z-
dc.date.available2018-10-11T02:51:45Z-
dc.date.issued2018-08-30-
dc.identifier.citationMolecules (Basel, Switzerland) 2018; 23(9): E2191en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/19599-
dc.description.abstractThe epithelium-specific ETS (ESE) transcription factors (ELF3, ELF5, EHF and SPDEF) are defined by their highly conserved ETS DNA binding domain and predominant epithelial-specific expression profile. ESE transcription factors maintain normal cell homeostasis and differentiation of a number of epithelial tissues, and their genetic alteration and deregulated expression has been linked to the progression of several epithelial cancers. Herein we review the normal function of the ESE transcription factors, the mechanisms by which they are dysregulated in cancers, and the current evidence for their role in cancer progression. Finally, we discuss potential therapeutic strategies for targeting or reactivating these factors as a novel means of cancer treatment.en
dc.language.isoeng-
dc.subjectEHFen
dc.subjectELF3en
dc.subjectELF5en
dc.subjectSPDEFen
dc.subjectCanceren
dc.subjecttranscription factoren
dc.titleELF3, ELF5, EHF and SPDEF Transcription Factors in Tissue Homeostasis and Cancer.en
dc.typeJournal Articleen
dc.identifier.journaltitleMolecules (Basel, Switzerland)en
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Bundoora, Victoria 3086, Australiaen
dc.identifier.doi10.3390/molecules23092191en
dc.type.contentTexten
dc.identifier.orcid0000-0001-9123-7684en
dc.identifier.pubmedid30200227-
dc.type.austinJournal Article-
dc.type.austinReview-
local.name.researcherMariadason, John M
item.languageiso639-1en-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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