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Promoting E2F1-mediated apoptosis in oestrogen receptor-alpha-negative breast cancer cells.

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dc.contributor.authorMaría del Mar Collado-González
dc.contributor.authorMaría Piedad Fernández-Pérez
dc.contributor.authorManel B Hammouda
dc.contributor.authorLana Tolordava
dc.contributor.authorMariam Gamkrelidze
dc.contributor.authorCollado-González, Mar
dc.contributor.authorMontenegro Arce, María Fernanda
dc.contributor.authorRodríguez López, José Neptuno
dc.contributor.departmentBioquímica y Biología Molecular A
dc.contributor.otherFacultades de la UMU
dc.date.accessioned2025-09-25T06:50:50Z
dc.date.available2025-09-25T06:50:50Z
dc.date.issued2014-07-14
dc.description.abstractBackground: Because oestrogen receptor α (ERα) regulates E2F1 expression to mediate tamoxifen resistance in ERα-positive breast cancer cells, we aimed to define the possible roles of ERα and E2F1 in promoting the resistance of ERα-negative breast cancer cells to 4-hydroxy-tamoxifen (4OHT). Methods: This study utilised conventional techniques to demonstrate the effects of 4OHT on the expression of ERα and E2F1 and also examined the individual and combined effects of 4OHT with dipyridamole (DIPY) and 3-O-(3,4,5-trimethoxybenzoyl)-(-)-catechin (TMCG) on the oestrogen-negative MDA-MB-231 breast cancer cell line using viability assays, Hoechst staining, MALDI-TOF mass spectroscopy, and confocal microscopy. Results: Despite the ERα-negative status of the MDA-MB-231 cells, we observed that 4OHT efficiently up-regulated ERα in these cells and that this upregulation promoted E2F1-mediated cell growth. Because E2F1 plays a dual role in cell growth/apoptosis, we designed a therapy incorporating TMCG/DIPY to take advantage of the elevated E2F1 expression in these 4OHT-treated cells. 4OHT enhances the toxicity of TMCG/DIPY in these ERα-negative breast cancer cells. Conclusions: Because TMCG/DIPY treatment modulates the methylation status/stability of E2F1, the results demonstrate that therapies targeting the epigenetic machinery of cancer cells in the presence of verexpressed E2F1 may result in efficient E2F1-mediated cell death.
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dc.identifier.citationBMC Cancer 2014, 14:539
dc.identifier.doi10/1186/1471-2407-14-539.
dc.identifier.issn1471-2407
dc.identifier.urihttp://hdl.handle.net/10201/159809
dc.languageeng
dc.relationThis work was supported by grants from Ministerio de Ciencia e Innovación (MICINN) (SAF2009-12043-C02-01), Fundación Séneca, Región de Murcia (FS-RM) (15230/PI/10), and EU ERA293514. M.F.M is contracted by Fundación Científica de la Asociación Española contra el Cáncer (FCAECC).
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titlePromoting E2F1-mediated apoptosis in oestrogen receptor-alpha-negative breast cancer cells.
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublicationes
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relation.isAuthorOfPublication.latestForDiscoveryba32f760-d55c-40a7-9452-62dfd47cbeaf
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