Exploring and Exploiting the Protein S100A7 as a New Target for Breast Cancer Therapy

Abstract

The following is a brief summary of the most significant achievement described herein: The conditions and mechanisms regulating S100A7 expression in breast cancer cells are not well understood. Because inflammation can regulate S100A7 in skin cells, we treated breast tumor cells with several inflammatory cytokines, including oncostatin-M (OSM), interleukin-6 (IL-6), TNF-alpha, and IL-Beta. Each of these could enhance S100A7 protein levels; however, OSM was by far the strongest inducer of S100A7 in breast cells and induced S100A7 at both the mRNA and protein levels. We noted that signaling by STAT3, PI3K and ERK1/2 were all necessary for OSM-induction of S100A7. The enhanced migratory rate bestowed by OSM stimulation was found to be dependent on S100A7. Finally, we observed that expression of S100A7 and OSM (and its receptor OSMR) were correlated in vivo, and that S100A7 may be correlated with poor patient prognosis only in the context of breast cancers that express OSMR.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Jan 01, 2010
Accession Number
ADA520729

Entities

People

  • Nathan West

Organizations

  • BC Cancer Agency

Tags

DTIC Thesaurus Topics

  • Adaptive Immunity
  • Biological Factors
  • Breast Cancer
  • Cell Line
  • Cell Movement
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Culture Media
  • Epithelial Cells
  • Fungi
  • Lymphocytes
  • Molecules
  • Neoplasms
  • Peptides
  • Proteins
  • Tumor Cell Line

Readers

  • Breast cancer cell signaling and growth regulation.
  • Oncology (Cancer Research).
  • Team-Based Human-Centered Cognitive Task Decision Making and Information Performance.