Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells
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...
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_19492553_v8_n51_p88475_Cambados |
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todo:paper_19492553_v8_n51_p88475_Cambados2023-10-03T16:37:19Z Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells Cambados, N. Walther, T. Nahmod, K. Tocci, J.M. Rubinstein, N. Böhme, I. Simian, M. Sampayo, R. Suberbordes, M.D.V. Kordon, E.C. Schere-Levy, C. AKT Angiotensin II Angiotensin-(1-7) Breast cancer cells Epithelial-mesenchymal transition alpha smooth muscle actin angiotensin 1 receptor angiotensin II angiotensin[1-7] fibronectin messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 nerve cell adhesion molecule phosphatidylinositol 3 kinase protein kinase B uvomorulin vasculotropin angiogenesis animal cell Article breast cancer breast epithelium cell cancer inhibition carcinogenicity cell invasion cell survival cell transformation controlled study enzyme activation enzyme activity epithelial mesenchymal transition human human cell MDA-MB-231 cell line metastasis inhibition migration inhibition mouse nonhuman protein expression signal transduction 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. © Cambados et al. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_19492553_v8_n51_p88475_Cambados |
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Universidad de Buenos Aires |
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I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
AKT Angiotensin II Angiotensin-(1-7) Breast cancer cells Epithelial-mesenchymal transition alpha smooth muscle actin angiotensin 1 receptor angiotensin II angiotensin[1-7] fibronectin messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 nerve cell adhesion molecule phosphatidylinositol 3 kinase protein kinase B uvomorulin vasculotropin angiogenesis animal cell Article breast cancer breast epithelium cell cancer inhibition carcinogenicity cell invasion cell survival cell transformation controlled study enzyme activation enzyme activity epithelial mesenchymal transition human human cell MDA-MB-231 cell line metastasis inhibition migration inhibition mouse nonhuman protein expression signal transduction |
| spellingShingle |
AKT Angiotensin II Angiotensin-(1-7) Breast cancer cells Epithelial-mesenchymal transition alpha smooth muscle actin angiotensin 1 receptor angiotensin II angiotensin[1-7] fibronectin messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 nerve cell adhesion molecule phosphatidylinositol 3 kinase protein kinase B uvomorulin vasculotropin angiogenesis animal cell Article breast cancer breast epithelium cell cancer inhibition carcinogenicity cell invasion cell survival cell transformation controlled study enzyme activation enzyme activity epithelial mesenchymal transition human human cell MDA-MB-231 cell line metastasis inhibition migration inhibition mouse nonhuman protein expression signal transduction Cambados, N. Walther, T. Nahmod, K. Tocci, J.M. Rubinstein, N. Böhme, I. Simian, M. Sampayo, R. Suberbordes, M.D.V. Kordon, E.C. Schere-Levy, C. Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| topic_facet |
AKT Angiotensin II Angiotensin-(1-7) Breast cancer cells Epithelial-mesenchymal transition alpha smooth muscle actin angiotensin 1 receptor angiotensin II angiotensin[1-7] fibronectin messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 nerve cell adhesion molecule phosphatidylinositol 3 kinase protein kinase B uvomorulin vasculotropin angiogenesis animal cell Article breast cancer breast epithelium cell cancer inhibition carcinogenicity cell invasion cell survival cell transformation controlled study enzyme activation enzyme activity epithelial mesenchymal transition human human cell MDA-MB-231 cell line metastasis inhibition migration inhibition mouse nonhuman protein expression signal transduction |
| description |
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. © Cambados et al. |
| format |
JOUR |
| author |
Cambados, N. Walther, T. Nahmod, K. Tocci, J.M. Rubinstein, N. Böhme, I. Simian, M. Sampayo, R. Suberbordes, M.D.V. Kordon, E.C. Schere-Levy, C. |
| author_facet |
Cambados, N. Walther, T. Nahmod, K. Tocci, J.M. Rubinstein, N. Böhme, I. Simian, M. Sampayo, R. Suberbordes, M.D.V. Kordon, E.C. Schere-Levy, C. |
| author_sort |
Cambados, N. |
| title |
Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| title_short |
Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| title_full |
Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| title_fullStr |
Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| title_full_unstemmed |
Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells |
| title_sort |
angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin ii in breast cancer cells |
| url |
http://hdl.handle.net/20.500.12110/paper_19492553_v8_n51_p88475_Cambados |
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