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Open Access Green as soon as Postprint is submitted to ZB.
Endothelial CCR2 signaling induced by colon carcinoma cells enables extravasation via the JAK2-Stat5 and p38MAPK pathway.
Cancer Cell 22, 91-105 (2012)
Increased expression of the chemokine CCL2 in tumor cells correlates with enhanced metastasis, poor prognosis, and recruitment of CCR2(+)Ly6C(hi) monocytes. However, the mechanisms driving tumor cell extravasation through the endothelium remain elusive. Here, we describe CCL2 upregulation in metastatic UICC stage IV colon carcinomas and demonstrate that tumor cell-derived CCL2 activates the CCR2(+) endothelium to increase vascular permeability in vivo. CCR2 deficiency prevents colon carcinoma extravasation and metastasis. Of note, CCR2 expression on radio-resistant cells or endothelial CCR2 expression restores extravasation and metastasis in Ccr2(-/-) mice. Reduction of CCR2 expression on myeloid cells decreases but does not prevent metastasis. CCL2-induced vascular permeability and metastasis is dependent on JAK2-Stat5 and p38MAPK signaling. Our study identifies potential targets for treating CCL2-dependent metastasis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
CHEMOKINE RECEPTOR 2; INFLAMMATORY MONOCYTES; TUMOR-METASTASIS; MYELOID CELLS; CANCER-CELLS; L-SELECTIN; MICE; CCL2; MIGRATION; LUNG
ISSN (print) / ISBN
1535-6108
e-ISSN
1878-3686
Journal
Cancer Cell
Quellenangaben
Volume: 22,
Issue: 1,
Pages: 91-105
Publisher
Cell Press
Publishing Place
Cambridge, Mass.
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)