Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells

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dc.contributor.author Cambados, Nadia
dc.contributor.author Walther, Thomas
dc.contributor.author Nahmod, Karen
dc.contributor.author Tocci, Johanna M.
dc.contributor.author Rubinstein, Natalia
dc.contributor.author Boehme, Ilka
dc.contributor.author Simian, Marina
dc.contributor.author Sampayo, Rocio
dc.contributor.author Del Valle Suberbordes, Melisa
dc.contributor.author Kordon, Edith C.
dc.contributor.author Schere-Levy, Carolina
dc.date.accessioned 2018-06-15T11:47:15Z
dc.date.available 2018-06-15T11:47:15Z
dc.date.issued 2017
dc.identifier.citation Cambados, N., Walther, T., Nahmod, K., Tocci, J. M., Rubinstein, N., Böhme, I., Simian, M., Sampayo, R., Suberbordes, M. D. V. and Kordon, E. C. (2017) 'Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells', Oncotarget, 8(51), pp. 88475-88487. doi: 10.18632/oncotarget.19290 en
dc.identifier.volume 8
dc.identifier.issued 51
dc.identifier.startpage 88475
dc.identifier.endpage 88487
dc.identifier.issn 1949-2553
dc.identifier.uri http://hdl.handle.net/10468/6340
dc.identifier.doi 10.18632/oncotarget.19290
dc.description.abstract Angiotensin (Ang) II, the main effector peptide of the renin-angiotensin system, has been implicated in multiple aspects of cancer progression such as proliferation, migration, invasion, angiogenesis and metastasis. Ang-(1-7), is a biologically active heptapeptide, generated predominantly from AngII by the enzymatic activity of angiotensin converting enzyme 2. Previous studies have shown that Ang-(1-7) counterbalances AngII actions in different pathophysiological settings. In this study, we have analysed the impact of Ang( 1-7) on AngII-induced pro-tumorigenic features on normal murine mammary epithelial cells NMuMG and breast cancer cells MDA-MB-231. AngII stimulated the activation of the survival factor AKT in NMuMG cells mainly through the AT1 receptor. This PI3K/AKT pathway activation also promoted epithelial-mesenchymal transition (EMT). Concomitant treatment of NMuMG cells with AngII and Ang-(1-7) completely abolished EMT features induced by AngII. Furthermore, Ang-(1-7) abrogated AngII induced migration and invasion of the MDA-MB-231 cells as well as pro-angiogenic events such as the stimulation of MMP-9 activity and VEGF expression. Together, these results demonstrate for the first time that Ang-(1-7) counteracts tumor aggressive signals stimulated by AngII in breast cancer cells emerging the peptide as a potential therapy to prevent breast cancer progression. en
dc.description.sponsorship Agencia Nacional de Promoción Científica y Tecnológica (PICT 2011-1638); Consejo Nacional de Investigaciones Científicas y Técnicas (Proyectos de Investigación Plurianuales); Ministerio de Ciencia, Tecnología e Innovación Productiva (Deutscher Akademischer Austauschdienst (DA1203); Deutsche Forschungsgemeinschaft (WA 1441/22-2) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Impact Journals en
dc.relation.uri http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=19290&path[]=61725
dc.rights © 2017, Cambados et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. en
dc.rights.uri http://creativecommons.org/licenses/by/3.0/
dc.subject AKT en
dc.subject Angiotensin ii en
dc.subject Angiotensin-(1-7) en
dc.subject Breast cancer cells en
dc.subject Epithelial-mesenchymal transition en
dc.title Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Thomas Walther, Pharmacology & Therapeutics, University College Cork, Cork, Ireland. +353-21-490-3000 Email: t.walther@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.contributor.funder Deutsche Forschungsgemeinschaft
dc.contributor.funder Ministerio de Ciencia, Tecnología e Innovación Productiva
dc.contributor.funder National Cancer Institute
dc.contributor.funder Consejo Nacional de Investigaciones Científicas y Técnicas
dc.contributor.funder Agencia Nacional de Promoción Científica y Tecnológica
dc.description.status Peer reviewed
dc.identifier.journaltitle Oncotarget en
dc.internal.IRISemailaddress t.walther@ucc.ie en


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© 2017, Cambados et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Except where otherwise noted, this item's license is described as © 2017, Cambados et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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