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http://hdl.handle.net/10261/169077
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dc.contributor.author | Orive-Ramos, Ana | - |
dc.contributor.author | Seoane, Samuel | - |
dc.contributor.author | Ocaña, Alberto | - |
dc.contributor.author | Pandiella, Atanasio | - |
dc.contributor.author | Montero, Juan Carlos | - |
dc.date.accessioned | 2018-08-23T09:33:21Z | - |
dc.date.available | 2018-08-23T09:33:21Z | - |
dc.date.issued | 2017 | - |
dc.identifier | doi: 10.1002/1878-0261.12145 | - |
dc.identifier | e-issn: 1878-0261 | - |
dc.identifier | issn: 1574-7891 | - |
dc.identifier.citation | Molecular Oncology 11(12): 1788-1805 (2017) | - |
dc.identifier.uri | http://hdl.handle.net/10261/169077 | - |
dc.description.abstract | Metastatic dissemination of tumor cells is responsible for the fatal outcome of breast cancer. Therefore, understanding the mechanisms involved in dissemination is essential for the development of new therapeutic strategies to prevent metastasis. One mechanism involved in metastatic dissemination of breast cancer cells is dependent on control of the production of matrix metalloproteinases by the neuregulins (NRGs). The NRGs are polypeptide factors that act by binding to the ErbB/HER subfamily of receptor tyrosine kinases. NRG-mediated activation of HER receptors causes an increase in the production of metalloprotease 13 (MMP13, also termed collagenase-3), which facilitates metastatic dissemination of breast tumors. In this context, we aimed to explore whether the clinically approved tyrosine kinase inhibitor dasatinib was able to neutralize this mechanism of metastatic dissemination. Here, we show that dasatinib restricted NRG-induced MMP13 upregulation, both in vitro and in vivo, and in vivo metastatic dissemination of breast cancer cells. Chemical proteomics studies showed that the main cellular targets of dasatinib were SRC family kinases (SFKs). Moreover, genetic studies showed that knockdown of SRC or YES strongly inhibited NRG-induced MMP13 upregulation in vitro. Mechanistically, dasatinib treatment or knockdown of SRC also inhibited ERK1/2 kinases in vitro, which were required for NRG-induced MMP13 upregulation. These results open the possibility of clinically exploring the antitumoral action of dasatinib in those tumors in which the NRG–MMP13 signaling axis may play a relevant role in the control of tumor cell dissemination. | - |
dc.description.sponsorship | AOR is the recipient of a predoctoral contract from the University of Salamanca. JCM is funded by the Instituto de Salud Carlos III through a Miguel Servet program (CP12/03073) and receives research support from the same institution (PI15/00684). The authors’ research in AP laboratory is supported by grants from the Ministry of Economy and Competitiveness of Spain (BFU2012-39151 and BFU2015-71371-R), the Instituto de Salud Carlos III through the Spanish Cancer Centers Network Program (RD12/0036/0003), the Scientific Foundation of the Spanish Association Against Cancer (AECC), and the CRIS Cancer Foundation. AO laboratory is funded by the Instituto de Salud Carlos III (PI16/01121), Diputacion de Albacete, and ACEPAIN. The IBMCC-CIC and the work carried out at our laboratories receive support from the European Community through the Regional Development Funding Program (FEDER). | - |
dc.publisher | John Wiley & Sons | - |
dc.publisher | Federation of European Biochemical Societies | - |
dc.relation | info:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/BFU2015-71371-R | - |
dc.relation.isversionof | Publisher's version | - |
dc.rights | openAccess | - |
dc.subject | Breast cancer dissemination | - |
dc.subject | SRC | - |
dc.subject | Dasatinib | - |
dc.subject | MMP13 | - |
dc.subject | Neuregulin | - |
dc.title | Regulation of the prometastatic neuregulin–MMP13 axis by SRC family kinases: therapeutic implications | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1002/1878-0261.12145 | - |
dc.relation.publisherversion | https://doi.org/10.1002/1878-0261.12145 | - |
dc.date.updated | 2018-08-23T09:33:21Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.rights.license | http://creativecommons.org/licenses/by/4.0/ | - |
dc.contributor.funder | Fundación Científica Asociación Española Contra el Cáncer | - |
dc.contributor.funder | Fundación CRIS contra el Cáncer | - |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | - |
dc.contributor.funder | European Commission | - |
dc.contributor.funder | Diputación de Albacete | - |
dc.contributor.funder | Universidad de Salamanca | - |
dc.contributor.funder | Instituto de Salud Carlos III | - |
dc.contributor.funder | Red Temática de Investigación Cooperativa en Cáncer (España) | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100002704 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100003329 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100000780 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004587 | es_ES |
dc.identifier.pmid | 29032615 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.fulltext | With Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
Aparece en las colecciones: | (IBMCC) Artículos |
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reguSRCimpli.pdf | 1,76 MB | Adobe PDF | Visualizar/Abrir |
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