Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/34802
Title: Angiotensin II Facilitates Breast Cancer Cell Migration and Metastasis
Authors: Rodrigues-Ferreira, Sylvie
Abdelkarim, Mohamed
Dillenburg-Pilla, Patricia
Luissint, Anny-Claude
di-Tommaso, Anne
Deshayes, Frederique
Pontes, Carmen Lucia S.
Molina, Angie
Cagnard, Nicolas
Letourneur, Franck
Morel, Marina
Reis, Rosana I.
Casarini, Dulce Elena [UNIFESP]
Terris, Benoit
Couraud, Pierre-Olivier
Costa-Neto, Claudio M.
Di Benedetto, Melanie
Nahmias, Clara
INSERM
Univ Paris 05
Univ Paris 13
CNRS
Universidade de São Paulo (USP)
Universidade Federal de São Carlos (UFSCar)
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 20-Apr-2012
Publisher: Public Library Science
Citation: Plos One. San Francisco: Public Library Science, v. 7, n. 4, 8 p., 2012.
Abstract: Breast cancer metastasis is a leading cause of death by malignancy in women worldwide. Efforts are being made to further characterize the rate-limiting steps of cancer metastasis, i.e. extravasation of circulating tumor cells and colonization of secondary organs. in this study, we investigated whether angiotensin II, a major vasoactive peptide both produced locally and released in the bloodstream, may trigger activating signals that contribute to cancer cell extravasation and metastasis. We used an experimental in vivo model of cancer metastasis in which bioluminescent breast tumor cells (D3H2LN) were injected intra-cardiacally into nude mice in order to recapitulate the late and essential steps of metastatic dissemination. Real-time intravital imaging studies revealed that angiotensin II accelerates the formation of metastatic foci at secondary sites. Pre-treatment of cancer cells with the peptide increases the number of mice with metastases, as well as the number and size of metastases per mouse. in vitro, angiotensin II contributes to each sequential step of cancer metastasis by promoting cancer cell adhesion to endothelial cells, trans-endothelial migration and tumor cell migration across extracellular matrix. At the molecular level, a total of 102 genes differentially expressed following angiotensin II pretreatment were identified by comparative DNA microarray. Angiotensin II regulates two groups of connected genes related to its precursor angiotensinogen. Among those, up-regulated MMP2/MMP9 and ICAM1 stand at the crossroad of a network of genes involved in cell adhesion, migration and invasion. Our data suggest that targeting angiotensin II production or action may represent a valuable therapeutic option to prevent metastatic progression of invasive breast tumors.
URI: http://repositorio.unifesp.br/handle/11600/34802
ISSN: 1932-6203
Other Identifiers: http://dx.doi.org/10.1371/journal.pone.0035667
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