Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/109923
DC Field | Value | Language |
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dc.contributor.author | Amaral, Cristina | - |
dc.contributor.author | Borges, Margarida | - |
dc.contributor.author | Melo, Soraia | - |
dc.contributor.author | Silva, Elisiário Tavares da | - |
dc.contributor.author | Correia-da-Silva, Georgina | - |
dc.contributor.author | Teixeira, Natércia A. A. | - |
dc.date.accessioned | 2023-11-07T10:42:57Z | - |
dc.date.available | 2023-11-07T10:42:57Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 1932-6203 | pt |
dc.identifier.uri | http://hdl.handle.net/10316/109923 | - |
dc.description.abstract | Aromatase inhibitors (AIs), which block the conversion of androgens to estrogens, are used for hormone-dependent breast cancer treatment. Exemestane, a steroidal that belongs to the third-generation of AIs, is a mechanism-based inhibitor that binds covalently and irreversibly, inactivating and destabilizing aromatase. Since the biological effects of exemestane in breast cancer cells are not totally understood, its effects on cell viability, cell proliferation and mechanisms of cell death were studied in an ER-positive aromatase-overexpressing breast cancer cell line (MCF-7aro). The effects of 3-methyladenine (3-MA), an inhibitor of autophagy and of ZVAD-FMK, an apoptotic inhibitor, in exemestane treated cells were also investigated. Our results indicate that exemestane induces a strong inhibition in MCF-7aro cell proliferation in a dose- and time-dependent manner, promoting a significant cell cycle arrest in G(0)/G1 or in G(2)/M phases after 3 and 6 days of treatment, respectively. This was accompanied by a decrease in cell viability due to activation of cell death by apoptosis, via mitochondrial pathway and the occurrence of autophagy. Inhibition of autophagy by the autophagic inhibitor, 3-MA, resulted in a reduction of cell viability and activation of caspases. All together the results obtained suggest that exemestane induced mitochondrial-mediated apoptosis and autophagy, which act as a pro-survival process regulating breast cancer cell apoptosis. | pt |
dc.language.iso | eng | pt |
dc.publisher | Public Library of Science | pt |
dc.relation | SFRH/BD/48190/2008 | pt |
dc.relation | FCOMP-01-0124-FEDER-020970 (PTDC/QUI-BIQ/120319/2010) | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject.mesh | Androstadienes | pt |
dc.subject.mesh | Antineoplastic Agents | pt |
dc.subject.mesh | Apoptosis | pt |
dc.subject.mesh | Aromatase | pt |
dc.subject.mesh | Autophagy | pt |
dc.subject.mesh | Breast Neoplasms | pt |
dc.subject.mesh | Cell Cycle | pt |
dc.subject.mesh | Cell Line, Tumor | pt |
dc.subject.mesh | Cell Proliferation | pt |
dc.subject.mesh | Cell Survival | pt |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | pt |
dc.subject.mesh | Humans | pt |
dc.subject.mesh | Receptors, Estrogen | pt |
dc.title | Apoptosis and autophagy in breast cancer cells following exemestane treatment | pt |
dc.type | article | - |
degois.publication.firstPage | e42398 | pt |
degois.publication.issue | 8 | pt |
degois.publication.title | PLoS ONE | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.1371/journal.pone.0042398 | pt |
degois.publication.volume | 7 | pt |
dc.date.embargo | 2012-01-01 | * |
uc.date.periodoEmbargo | 0 | pt |
item.fulltext | Com Texto completo | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.languageiso639-1 | en | - |
item.openairetype | article | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0002-0390-3403 | - |
Appears in Collections: | FCTUC Ciências da Vida - Artigos em Revistas Internacionais FFUC- Artigos em Revistas Internacionais |
Files in This Item:
File | Description | Size | Format | |
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Apoptosis-and-autophagy-in-breast-cancer-cells-following-exemestane-treatmentPLoS-ONE.pdf | 1.68 MB | Adobe PDF | View/Open |
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