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

Thomas J. Wilson, Kalyan C. Nannuru, Mitsuru Futakuchi, Rakesh K. Singh

Research output: Contribution to journalArticle

48 Scopus citations

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 languageEnglish (US)
Pages (from-to)162-169
Number of pages8
JournalCancer Letters
Volume288
Issue number2
DOIs
StatePublished - Feb 28 2010

Keywords

  • Angiogenesis
  • Bone metastasis
  • Breast cancer
  • Cathepsin G
  • TGF-β

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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