Publication:
SIRT1 and estrogen signaling cooperation for breast cancer onset and progression

dc.contributor.authorLiarte, Sergio
dc.contributor.authorAlonso-Romero, José Luis
dc.contributor.authorNicolás, Francisco José
dc.contributor.departmentMedicina
dc.date.accessioned2024-11-07T12:36:11Z
dc.date.available2024-11-07T12:36:11Z
dc.date.issued2018-09-27
dc.description© 2018 Liarte, Alonso-Romero and Nicolás. This manuscript version is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by/4.0/. This document is the Published version of a Published Work that appeared in final form in Frontiers in Endocrinology. To access the final edited and published work see https://doi.org/10.3389/fendo.2018.00552
dc.description.abstractBreast cancer remains a significant female mortality cause. It constitutes a multifactorial disease for which research on environmental factors offers little help in predicting onset or progression. The pursuit for its foundations by analyzing hormonal changes as a motive for disease development, indicates that increased exposure to estrogens associates with increased risk. A prevalent number of breast cancer cases show dependence on the increased activity of the classic nuclear estrogen receptor (ER) for cell proliferation and survival. SIRT1 is a Type III histone deacetylase which is receiving increasing attention due to its ability to perform activities over relevant non-histone proteins and transcription factors. Interestingly, concomitant SIRT1 overexpression is commonly found in ER-positive breast cancer cases. Both proteins had been shown to directly interact, in a process related to altered intracellular signaling and aberrant transcription, then promoting tumor progression. Moreover, SIRT1 activities had been also linked to estrogenic effects through interaction with the G-protein coupled membrane bound estrogen receptor (GPER). This work aims to summarize present knowledge on the interplay between SIRT1 and ER/GPER for breast cancer onset and progression. Lastly, evidences on the ability of SIRT1 to interact with TGFß signaling, a concurrent pathway significantly involved in breast cancer progression, are reported. The potential of this research field for the development of innovative strategies in the assessment of orphan breast cancer subtypes, such as triple negative breast cancer (TNBC), is discussed.es
dc.formatapplication/pdfes
dc.format.extent9es
dc.identifier.citationFront. Endocrinol. 9:552
dc.identifier.doihttps://doi.org/10.3389/fendo.2018.00552
dc.identifier.issnElectronic: 1664-2392
dc.identifier.urihttp://hdl.handle.net/10201/146067
dc.languageenges
dc.publisherFrontiers Media
dc.relationThis work was supported by grants (SAF2006–09482; SAF2003– 06029) from the Spanish Ministry of Education and Science. Also, this work was supported by a grant (PI13/00794) from the Instituto de Salud Carlos III. And the Fondos FEDER Una manera de hacer Europa (ERDF, A way to build Europe). SL received a fellowship from Roche. FN was supported the Fundación para la Formación e Investigación Sanitarias de la Región de Murcia.es
dc.relation.publisherversionhttps://digitum.um.es/digitum/retrieve/654917
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectSIRT1es
dc.subjectSex steroidses
dc.subjectEstrogen receptores
dc.subjectGPERes
dc.subjectBreast canceres
dc.subjectTNBCes
dc.titleSIRT1 and estrogen signaling cooperation for breast cancer onset and progressiones
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
Files
Original bundle
Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
fendo-09-00552.pdf
Size:
799.64 KB
Format:
Adobe Portable Document Format
Description:
License bundle
Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
license.txt
Size:
2.26 KB
Format:
Item-specific license agreed upon to submission
Description:
Collections