Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/51686

TitleLoss of Caveolin-1 in Metastasis-Associated Macrophages Drives Lung Metastatic Growth through Increased Angiogenesis
Author(s)Celus, Ward
Conza, Giusy Di
Oliveira, Ana Isabel Ferreira
Ehling, Manuel
Costa, Bruno Marques
Wenes, Mathias
Mazzone, Massimiliano
KeywordsCaveolin-1
Macrophages
Metastasis
Angiogenesis
MMP9
VEGFR1
CSF1
VEGF-A
Issue date13-Dec-2017
PublisherElsevier
JournalCell Reports
CitationCelus, W., Di Conza, G., Oliveira, A. I., Ehling, M., Costa, B. M., Wenes, M., & Mazzone, M. (2017). Loss of Caveolin-1 in Metastasis-Associated Macrophages Drives Lung Metastatic Growth through Increased Angiogenesis. Cell reports, 21(10), 2842-2854
Abstract(s)Although it is well established that tumor-associated macrophages take part in each step of cancer progression, less is known about the distinct role of the so-called metastasis-associated macrophages (MAMs) at the metastatic site. Previous studies reported that Caveolin-1 (Cav1) has both tumor-promoting and tumor-suppressive functions. However, the role of Cav1 in bone-marrow-derived cells is unknown. Here, we describe Cav1 as an anti-metastatic regulator in mouse models of lung and breast cancer pulmonary metastasis. Among all the recruited inflammatory cell populations, we show that MAMs uniquely express abundant levels of Cav1. Using clodronate depletion of macrophages, we demonstrate that macrophage Cav1 signaling is critical for metastasis and not for primary tumor growth. In particular, Cav1 inhibition does not affect MAM recruitment to the metastatic site but, in turn, favors angiogenesis. We describe a mechanism by which Cav1 in MAMs specifically restrains vascular endothelial growth factor A/vascular endothelial growth factor receptor 1 (VEGF-A/VEGFR1) signaling and its downstream effectors, matrix metallopeptidase 9 (MMP9) and colony-stimulating factor 1 (CSF1).
TypeArticle
URIhttp://hdl.handle.net/1822/51686
DOI10.1016/j.celrep.2017.11.034
ISSN2211-1247
Publisher versionhttps://www.sciencedirect.com/science/article/pii/S2211124717316716
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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