2011
DOI: 10.1016/j.canlet.2010.09.020
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Activation of kinin B1 receptor increases the release of metalloproteases-2 and -9 from both estrogen-sensitive and -insensitive breast cancer cells

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Cited by 47 publications
(53 citation statements)
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“…MMP-9 is induced by adhesion molecules, mainly activated integrins, cytokines and growth factors (Beliveau et al, 2010;Zhao and Benveniste, 2008). As an example, cell binding to vitronectin or fibronectin trigger MMP-9 expression, IL-1b, TNF-a or TGF-b induce MMP-9 in a autocrine and paracrine fashion, EGF release or the aberrant activation of the EGFR result in over-expression of MMP-9 (Coulson-Thomas et al, 2010;Ehrenfeld et al, 2011;Ikari et al, 2011;Lin et al, 2009;Yu and Stamenkovic, 2000).…”
Section: Biological Aspectsmentioning
confidence: 99%
“…MMP-9 is induced by adhesion molecules, mainly activated integrins, cytokines and growth factors (Beliveau et al, 2010;Zhao and Benveniste, 2008). As an example, cell binding to vitronectin or fibronectin trigger MMP-9 expression, IL-1b, TNF-a or TGF-b induce MMP-9 in a autocrine and paracrine fashion, EGF release or the aberrant activation of the EGFR result in over-expression of MMP-9 (Coulson-Thomas et al, 2010;Ehrenfeld et al, 2011;Ikari et al, 2011;Lin et al, 2009;Yu and Stamenkovic, 2000).…”
Section: Biological Aspectsmentioning
confidence: 99%
“…For example, B1R induction is part of the proinflammatory phenotype promoted by low laminar shear stress and may participate in responses including vasodilatation and leukocyte recruitment in atherogenesis [8]. Furthermore, B1R is coupled to both proliferation [9] and the release of metaloproteinases in breast cancer cells [10] suggesting an involvement in cancer cell invasiveness. Thus, B1R is a promising therapeutic target in both renal and cardiovascular disease [11] and cancer [12].…”
Section: Introductionmentioning
confidence: 99%
“…We have also reported that release of metalloproteases in MCF-7 and MDA-MB-231 breast cancer cells was blocked by AG1478, an observation that was confirmed by transfection of breast cancer cells with the dominant negative EGFR mutant HERCD533 (Ehrenfeld et al, 2011). The transactivation mechanism involved in EGFR activation by B1R agonists has not been elucidated yet, but work performed by our group in human HaCaT keratinocytes, MCF-7 breast cancer cell has visualized that B1R stimulation produces Src phosphorylation, that is blocked by the specific Src inhibitor, PP2 (Figs.…”
Section: Mechanisms Of Egfr Transactivation By Kinin B1 Receptormentioning
confidence: 54%
“…Moreover, it is known that release of the kinin moiety from kininogens sited on the neutrophil surface by enzymatic action of the classical tissue kallikrein (hK1) results in opening of junctions between the endothelial cells, thereby causing plasma extravasation (Stuardo et al, 2004). B1R modulates the release of matrix metalloproteases from both human neutrophils ) and breast cancer cells (Ehrenfeld et al, 2011), an event that may contribute to the extracellular matrix remodeling in processes such as inflammation, wound healing and cancer. Part of the effects produced by B1R in neutrophils and cancer cells include activation of ERK1/2 and p38 MAPK and transactivation of EGFR in breast cancer cells, an event that usually results in the activation of MAPK.…”
Section: Wwwintechopencommentioning
confidence: 99%