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dc.contributor.authorAlasmael, N
dc.contributor.authorMohan, R
dc.contributor.authorMeira, LB
dc.contributor.authorSwales, KE
dc.contributor.authorPlant, NJ
dc.date.accessioned2018-07-05T09:58:20Z
dc.date.issued2016-01
dc.identifier.citationCancer letters, 2016, 370 (2), pp. 250 - 259
dc.identifier.issn0304-3835
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1990
dc.identifier.eissn1872-7980
dc.identifier.doi10.1016/j.canlet.2015.10.031
dc.description.abstractBreast cancer is the commonest form of cancer in women, but successful treatment is confounded by the heterogeneous nature of breast tumours: Effective treatments exist for hormone-sensitive tumours, but triple-negative breast cancer results in poor survival. An area of increasing interest is metabolic reprogramming, whereby drug-induced alterations in the metabolic landscape of a tumour slow tumour growth and/or increase sensitivity to existing therapeutics. Nuclear receptors are transcription factors central to the expression of metabolic and transport proteins, and thus represent potential targets for metabolic reprogramming. We show that activation of the nuclear receptor FXR, either by its endogenous ligand CDCA or the synthetic GW4064, leads to cell death in four breast cancer cell lines with distinct phenotypes: MCF-10A (normal), MCF-7 (receptor positive), MDA-MB-231 and MDA-MB-468 (triple negative). Furthermore, we show that the mechanism of cell death is predominantly through the intrinsic apoptotic pathway. Finally, we demonstrate that FXR agonists do not stimulate migration in breast cancer cell lines, an important potential adverse effect. Together, our data support the continued examination of FXR agonists as a novel class of therapeutics for the treatment of breast cancer.
dc.formatPrint-Electronic
dc.format.extent250 - 259
dc.languageeng
dc.language.isoeng
dc.subjectCell Line, Tumor
dc.subjectHumans
dc.subjectBreast Neoplasms
dc.subjectIsoxazoles
dc.subjectChenodeoxycholic Acid
dc.subjectReceptors, Cytoplasmic and Nuclear
dc.subjectApoptosis
dc.subjectCell Movement
dc.subjectAutophagy
dc.subjectFemale
dc.titleActivation of the Farnesoid X-receptor in breast cancer cell lines results in cytotoxicity but not increased migration potential.
dc.typeJournal Article
dcterms.dateAccepted2015-10-26
rioxxterms.versionofrecord10.1016/j.canlet.2015.10.031
rioxxterms.licenseref.startdate2016-01
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCancer letters
pubs.issue2
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Clinical PD Biomarker Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Clinical PD Biomarker Group
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Clinical PD Biomarker Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Clinical PD Biomarker Group
pubs.publication-statusPublished
pubs.volume370
pubs.embargo.termsNot known
icr.researchteamClinical PD Biomarker Groupen_US
dc.contributor.icrauthorSwales, Karenen


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