The cytoplasmic region of SARAF reduces triple-negative breast cancer metastasis through the regulation of store-operated calcium entryt
Author
dc.contributor.author
Saldías Maulén, María Paz
Author
dc.contributor.author
Cruz Núñez, Pablo
Author
dc.contributor.author
Silva Del Canto, Ian
Author
dc.contributor.author
Orellana Serradell, Octavio Andrés
Author
dc.contributor.author
Lavanderos Andrade, Boris Joan
Author
dc.contributor.author
Maureira Fuentes, Diego Javier
Author
dc.contributor.author
Pinto Sierralta, Raquel Cristina
Author
dc.contributor.author
Cerda Arancibia, Oscar Alejandro
Admission date
dc.date.accessioned
2024-07-11T21:07:13Z
Available date
dc.date.available
2024-07-11T21:07:13Z
Publication date
dc.date.issued
2023
Cita de ítem
dc.identifier.citation
Int. J. Mol. Sci. 2023, 24, 5306
es_ES
Identifier
dc.identifier.other
10.3390/ijms24065306
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/199552
Abstract
dc.description.abstract
Triple-negative breast cancer has a poor prognosis and is non-responsive to first-line therapies; hence, new therapeutic strategies are needed. Enhanced store-operated Ca2+ entry (SOCE) has been widely described as a contributing factor to tumorigenic behavior in several tumor types, particularly in breast cancer cells. SOCE-associated regulatory factor (SARAF) acts as an inhibitor of the SOCE response and, therefore, can be a potential antitumor factor. Herein, we generated a C-terminal SARAF fragment to evaluate the effect of overexpression of this peptide on the malignancy of triple-negative breast cancer cell lines. Using both in vitro and in vivo approaches, we showed that overexpression of the C-terminal SARAF fragment reduced proliferation, cell migration, and the invasion of murine and human breast cancer cells by decreasing the SOCE response. Our data suggest that regulating the activity of the SOCE response via SARAF activity might constitute the basis for further alternative therapeutic strategies for triple-negative breast cancer
es_ES
Lenguage
dc.language.iso
en
es_ES
Publisher
dc.publisher
MDPI
es_ES
Type of license
dc.rights
Attribution-NonCommercial-NoDerivs 3.0 United States