Abstract
Transforming growth factor (TGF)-β signaling makes a significant contribution to the pathogenesis of breast cancer bone metastasis. In other tumor types, TGF-β has been shown to promote tumor vascularity. Here, we report that inhibition of TGF-β 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-β signaling, and we also report that inhibition of Cathepsin G reduced tumor vascularity, as well as VEGF and MCP-1 expression.
Original language | English (US) |
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Pages (from-to) | 162-169 |
Number of pages | 8 |
Journal | Cancer Letters |
Volume | 288 |
Issue number | 2 |
DOIs | |
State | Published - Feb 28 2010 |
Keywords
- Angiogenesis
- Bone metastasis
- Breast cancer
- Cathepsin G
- TGF-β
ASJC Scopus subject areas
- Oncology
- Cancer Research