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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" (2017) Oncotarget. 8(51):88475-88487
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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. © Cambados et al.

Registro:

Documento: Artículo
Título:Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells
Autor: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.
Filiación:Instituto de Fisiología, Biología Molecular y Neurociencias, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Department of Obstetrics, University of Leipzig, Leipzig, Germany
Department of Pediatric Surgery, University of Leipzig, Leipzig, Germany
Department Pharmacology and Therapeutics, School of Medicine and School of Pharmacy, University College Cork, Cork, Ireland
Institute of Medical Biochemistry and Molecular Biology, University Medicine Greifswald, Greifswald, Germany
Department of Pediatrics, Immunology, Allergy and Rheumatology, Center for Human Immunobiology, Texas Children's Hospital, Houston, TX, United States
Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Instituto de Nanosistemas, Universidad Nacional de San Martín, Buenos Aires, Argentina
Departmento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Palabras clave: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
Año:2017
Volumen:8
Número:51
Página de inicio:88475
Página de fin:88487
DOI: http://dx.doi.org/10.18632/oncotarget.19290
Título revista:Oncotarget
Título revista abreviado:Oncotarget
ISSN:19492553
CAS:angiotensin II, 11128-99-7, 68521-88-0; angiotensin[1-7], 39386-80-6; fibronectin, 86088-83-7; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; phosphatidylinositol 3 kinase, 115926-52-8; protein kinase B, 148640-14-6; uvomorulin, 112956-45-3; vasculotropin, 127464-60-2
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_19492553_v8_n51_p88475_Cambados

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Citas:

---------- APA ----------
Cambados, N., Walther, T., Nahmod, K., Tocci, J.M., Rubinstein, N., Böhme, I., Simian, M.,..., Schere-Levy, C. (2017) . Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells. Oncotarget, 8(51), 88475-88487.
http://dx.doi.org/10.18632/oncotarget.19290
---------- CHICAGO ----------
Cambados, N., Walther, T., Nahmod, K., Tocci, J.M., Rubinstein, N., Böhme, I., et al. "Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells" . Oncotarget 8, no. 51 (2017) : 88475-88487.
http://dx.doi.org/10.18632/oncotarget.19290
---------- MLA ----------
Cambados, N., Walther, T., Nahmod, K., Tocci, J.M., Rubinstein, N., Böhme, I., et al. "Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells" . Oncotarget, vol. 8, no. 51, 2017, pp. 88475-88487.
http://dx.doi.org/10.18632/oncotarget.19290
---------- VANCOUVER ----------
Cambados, N., Walther, T., Nahmod, K., Tocci, J.M., Rubinstein, N., Böhme, I., et al. Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells. Oncotarget. 2017;8(51):88475-88487.
http://dx.doi.org/10.18632/oncotarget.19290