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http://hdl.handle.net/10261/51161
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Yerbes, Rosario | - |
dc.contributor.author | López-Rivas, Abelardo | - |
dc.date.accessioned | 2012-06-11T08:41:15Z | - |
dc.date.available | 2012-06-11T08:41:15Z | - |
dc.date.issued | 2012-04 | - |
dc.identifier | issn: 0167-6997 | - |
dc.identifier | e-issn: 1573-0646 | - |
dc.identifier.citation | Investigational New Drugs 30(2): 541-547 (2012) | - |
dc.identifier.uri | http://hdl.handle.net/10261/51161 | - |
dc.description.abstract | The histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA, vorinostat) is undergoing clinical trials as an antitumor drug and has received regulatory approval for cancer treatment. Here, we show that pre-treatment of human breast cancer cells with SAHA makes them susceptible to apoptosis induced by TRAIL (tumour necrosis factor-related apoptosis-inducing ligand). The apoptosis of breast tumour cells induced by TRAIL is blocked at the level of apical activation of caspase-8 and SAHA enhances the TRAIL-induced processing of procaspase-8. Consequently, a TRAIL associated pathway of apoptosis operated via mitochondria is activated in cells treated with SAHA. Interestingly, degradation of cellular FLICE-inhibitory proteins (cFLIPL and cFLIPS) by an ubiquitin/proteasome-dependent Itch/AIP4-independent mechanism is observed upon exposure to SAHA. Targeting cFLIPL directly with siRNA oligonucleotides also sensitizes human breast tumour cells to TRAIL-induced apoptosis. Furthermore, cFLIPL over-expression significantly inhibits the apoptosis elicited through the combined effects of SAHA and TRAIL. Together, these results indicate that SAHA sensitizes breast cancer cells to TRAIL-induced apoptosis by facilitating the activation of early events in the apoptotic TRAIL pathway. Therefore, the combination of TRAIL and SAHA may represent a therapeutic tool to combat breast tumours. | - |
dc.description.sponsorship | This work was supported by grants from Ministerio de Educación y Ciencia (SAF2006-00633 and SAF2009-07163), Red Temática de Investigación Cooperativa en Cáncer (RTICC: RD06/0020/0068) and Junta de Andalucía (CTS-211 and CVI-4497) to AL-R. RY was supported by contracts from Instituto de Salud Carlos III and Ministerio de Ciencia e Innovación. | - |
dc.language.iso | eng | - |
dc.publisher | Springer Nature | - |
dc.rights | closedAccess | - |
dc.subject | SAHA | - |
dc.subject | TRAIL | - |
dc.subject | Apoptosis | - |
dc.subject | Breast cancer cells | - |
dc.subject | cFLIP | - |
dc.subject | Itch/AIP4 | - |
dc.title | Itch/AIP4-independent proteasomal degradation of cFLIP mediates sensitization of breast tumor cells to TRAIL by the histone deacetylase inhibitor SAHA | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1007/s10637-010-9597-x | - |
dc.relation.publisherversion | http://dx.doi.org/10.1007/s10637-010-9597-x | - |
dc.date.updated | 2012-06-11T08:41:16Z | - |
dc.description.version | Peer Reviewed | - |
dc.contributor.funder | Ministerio de Educación y Ciencia (España) | - |
dc.contributor.funder | Red Temática de Investigación Cooperativa en Cáncer (España) | - |
dc.contributor.funder | Junta de Andalucía | - |
dc.contributor.funder | Instituto de Salud Carlos III | - |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004587 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004837 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100011011 | es_ES |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
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