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Cancer Lett. 2010 Feb 28;288(2):162-9. doi: 10.1016/j.canlet.2009.06.035. Epub 2009 Jul 30.

Cathepsin G-mediated enhanced TGF-beta signaling promotes angiogenesis via upregulation of VEGF and MCP-1.

Author information

1
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, 68198-5845, United States.

Abstract

Transforming growth factor (TGF)-beta signaling makes a significant contribution to the pathogenesis of breast cancer bone metastasis. In other tumor types, TGF-beta has been shown to promote tumor vascularity. Here, we report that inhibition of TGF-beta significantly reduces microvessel density in mammary tumor-induced bone lesions, mediated by decreased expression of both vascular endothelial growth factor (VEGF) and monocyte chemotactic protein (MCP)-1, both known angiogenic factors. Cathepsin G upregulation at the tumor-bone interface has been linked to increased TGF-beta signaling, and we also report that inhibition of Cathepsin G reduced tumor vascularity, as well as VEGF and MCP-1 expression.

PMID:
19646811
PMCID:
PMC2815079
DOI:
10.1016/j.canlet.2009.06.035
[Indexed for MEDLINE]
Free PMC Article

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