Anti-Estrogen Regulation of Macrophage Products that Influence Breast Cancer Cell Proliferation and Susceptibility to Apoptosis

Abstract

We have characterized the regulation of gene expression in MCF-7 breast cancer cells and THP-l macrophages as a model of epithelial cell-stromal cell interaction in breast cancer progression. THP-1 macrophages enhanced the proliferation of MCF-7 cells, protected them against tamoxifen killing, and induced the expression of several MCF-7 angiogenesis-related genes, including IL-8 (interleukin-8), OPN (osteopontin), MDK (Midkine), TGFRl/2/3 (TGF receptors 1, 2, 3), and 1D3 (inhibitor of differentiation 3). Pre-treatment of THP-l macrophages with 1 mM aspirin abrogated their protection of MCF-7 cells against tamoxifen killing, while down-regulating several angiogenesis-related genes in the macrophages. Reciprocally, MCF-7 cells altered the expression of angiogenesis-related genes in the macrophages: THP-1 macrophages expressed both vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) genes when cultured alone; however, in the presence of MCF-7 cells, PEDF expression was dramatically down-regulated. Because PEDF is a potent inhibitor of angiogenesis, the ability of MCF-7 cells to suppress PEDF expression in tumor-associated macrophages, while sustaining VEGF expression, may be a mechanism by which tumor cells regulate macrophage function to promote tumor growth.

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Document Details

Document Type
Technical Report
Publication Date
Aug 01, 2004
Accession Number
ADA431834

Entities

People

  • Theodore Bremner

Organizations

  • Howard University

Tags

DTIC Thesaurus Topics

  • Antineoplastic Agents
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Epithelial Cells
  • Gene Expression
  • Genetics
  • Growth Factors
  • Health Services
  • Medical Personnel
  • Molecular Biology
  • Neoplasms
  • Proteins
  • Stromal Cells
  • Tumor Cell Line

Fields of Study

  • Biology
  • Chemistry
  • Medicine

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology (Cancer Research).